Publications by authors named "Cong-Cong Zhang"

38 Publications

[Effect of arachidonic acid cytochrome P450ω hydroxylase Cyp4a14 gene knockout on skeletal muscle regeneration after injury].

Sheng Li Xue Bao 2021 Aug;73(4):577-583

Vascular Biology Department of Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Vascular Diseases, Beijing 100029, China.

The objective of this study was to explore the roles of arachidonic acid cytochrome P450ω hydroxylase CYP4A14 in skeletal muscle regeneration after injury. Wild-type (WT) control mice and Cyp4a14 knockout (A14) mice were used to establish the muscle injury and regeneration model by intramuscular injection with cardiotoxin (CTX) on the tibial anterior (TA) muscle. The TA muscles were harvested at the time points of 0, 3, 5 and 15 days after injury. The changes in skeletal muscle regeneration and fibrosis were assessed by wheat germ agglutinin (WGA) staining and Sirius Red staining. Immunohistochemical staining was used to observe the expression of proliferation-related protein Ki-67 and macrophage marker protein Mac-2. The mRNA levels of regeneration and inflammation associated genes were analyzed by real-time PCR. The results showed that the cross-section area (CSA) of regenerated myofibers in A14 mice was significantly smaller (P < 0.05), while the percentage of fibrosis area was significantly higher than those in WT mice at 15 days after injury (P < 0.05). In A14 muscles, both the ratio of Ki-67 positive proliferating cells and the mRNA levels of differentiation associated genes Myod1 and Myog were significantly lower than those in WT muscles (P < 0.05). At 3 days after injury, the mRNA expression of inflammatory cells marker genes CD45 and CD11b and Mac-2 positive macrophages in A14 muscles were significantly lower than those in WT skeletal muscle (P < 0.05). Macrophages derived pro-regeneration cytokines IL-1β, IGF-1 and SDF-1 were also significantly decreased in A14 muscles (P < 0.05). These results suggest that arachidonic acid cytochrome P450ω hydroxylase CYP4A14 plays a critical role in skeletal muscle regeneration after injury.
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August 2021

[Arachidonic acid Alox15/12-HETE signaling inhibits vascular calcification].

Sheng Li Xue Bao 2021 Aug;73(4):571-576

Vascular Biology Department of Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Vascular Diseases, Beijing 100029, China.

This study aims to explore the effects of arachidonic acid lipoxygenase metabolism in vascular calcification. We used 5/6 nephrectomy and high-phosphorus feeding to establish a model of vascular calcification in mice. Six weeks after nephrectomy surgery, vascular calcium content was measured, and Alizarin Red S and Von Kossa staining were applied to detect calcium deposition in aortic arch. Control aortas and calcified aortas were collected for mass spectrometry detection of arachidonic acid metabolites, and active molecules in lipoxygenase pathway were analyzed. Real-time quantitative PCR was used to detect changes in the expression of lipoxygenase in calcified aortas. Lipoxygenase inhibitor was used to clarify the effect of lipoxygenase metabolic pathways on vascular calcification. The results showed that 6 weeks after nephrectomy surgery, the aortic calcium content of the surgery group was significantly higher than that of the sham group (P < 0.05). Alizarin Red S staining and Von Kossa staining showed obvious calcium deposition in aortic arch from surgery group, indicating formation of vascular calcification. Nine arachidonic acid lipoxygenase metabolites were quantitated using liquid chromatography/mass spectrometry (LC-MS) analysis. The content of multiple metabolites (12-HETE, 11-HETE, 15-HETE, etc.) was significantly increased in calcified aortas, and the most abundant and up-regulated metabolite was 12-HETE. Furthermore, we examined the mRNA levels of metabolic enzymes that produce 12-HETE in calcified blood vessels and found the expression of arachidonate lipoxygenase-15 (Alox15) was increased. Blocking Alox15/12-HETE by Alox15 specific inhibitor PD146176 significantly decreased the plasma 12-HETE content, promoted calcium deposition in aortic arch and increased vascular calcium content. These results suggest that the metabolism of arachidonic acid lipoxygenase is activated in calcified aorta, and the Alox15/12-HETE signaling pathway may play a protective role in vascular calcification.
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August 2021

Identification of Dacinostat as a potential anti-obesity compound through transcriptional activation of adipose thermogenesis in mice.

Biochim Biophys Acta Mol Basis Dis 2021 Sep 15;1867(9):166169. Epub 2021 May 15.

Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China. Electronic address:

Obesity is a worldwide health problem. Activating fat mobilization and reducing fat synthesis is a promising strategy to mitigate obesity and its complicated metabolic diseases. However, few clinically effective and safe agents conform to the strategy. In the present study, by screening the next-generation L1000-based CMAP small molecule library, we identify histone deacetylase inhibitor Dacinostat, which has been previously tested in clinical trials for patients with advanced solid tumors, as an anti-obesity candidate. Administration of Dacinostat prevents high-fat diet-induced obesity, insulin resistance, and fatty liver in mice without causing adverse effects. Dacinostat treatment enhances adipose thermogenesis as shown by elevated body temperature, accompanied with high mRNA expression of Ucp1 and Ppargc1α. Mechanistically, we show that the thermogenic effect of Dacinostat is achieved by acetylation of histone 3 lysine 27 mediated transcriptional activation of Ucp1 and Ppargc1α in adipose tissue. In conclusion, these findings suggest that Dacinostat is a potential anti-obesity compound through transcriptional activation of adipose thermogenesis.
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http://dx.doi.org/10.1016/j.bbadis.2021.166169DOI Listing
September 2021

Comprehensive profiling and characterization of the absorbed components and metabolites in mice serum and tissues following oral administration of Qing-Fei-Pai-Du decoction by UHPLC-Q-Exactive-Orbitrap HRMS.

Chin J Nat Med 2021 Apr;19(4):305-320

Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. Electronic address:

Qing-Fei-Pai-Du decoction (QFPDD) is a Chinese medicine compound formula recommended for combating corona virus disease 2019 (COVID-19) by National Health Commission of the People's Republic of China. The latest clinical study showed that early treatment with QFPDD was associated with favorable outcomes for patient recovery, viral shedding, hospital stay, and course of the disease. However, the effective constituents of QFPDD remain unclear. In this study, an UHPLC-Q-Orbitrap HRMS based method was developed to identify the chemical constituents in QFPDD and the absorbed prototypes as well as the metabolites in mice serum and tissues following oral administration of QFPDD. A total of 405 chemicals, including 40 kinds of alkaloids, 162 kinds of flavonoids, 44 kinds of organic acids, 71 kinds of triterpene saponins and 88 kinds of other compounds in the water extract of QFPDD were tentatively identified via comparison with the retention times and MS/MS spectra of the standards or refereed by literature. With the help of the standards and in vitro metabolites, 195 chemical components (including 104 prototypes and 91 metabolites) were identified in mice serum after oral administration of QFPDD. In addition, 165, 177, 112, 120, 44, 53 constituents were identified in the lung, liver, heart, kidney, brain, and spleen of QFPDD-treated mice, respectively. These findings provided key information and guidance for further investigation on the pharmacologically active substances and clinical applications of QFPDD.
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http://dx.doi.org/10.1016/S1875-5364(21)60031-6DOI Listing
April 2021

[Chemical profiling and tissue distribution study of Jingyin Granules in rats using UHPLC-Q-Exactive Orbitrap HR-MS].

Zhongguo Zhong Yao Za Zhi 2020 Nov;45(22):5537-5554

Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine Shanghai 201203, China.

In this study, the chemical profiling of Jingyin Granules and the tissue distribution of nine major constituents in this Chinese medicine were performed after oral administration of Jingyin Granules to rats, by using UHPLC-Q-Exactive Orbitrap HR-MS. An Acquity UPLC BEH C_(18) chromatographic column(2.1 mm×100 mm, 1.7 μm) was used as solid phase, while the mobile phase was methanol and 0.1% formic acid water for gradient elution. The major constituents in this Chinese medicine were quickly and accurately identified, via comparison with the retention times and MS/MS spectra of the standards. A total of 106 chemicals were identified from Jingyin Granules, including 24 kinds of organic acids, 47 kinds of flavonoids, 10 kinds of iridoids, and 21 kinds of saponins and 4 kinds of other compounds. After oral administered Jingyin Granules to rats, 48, 30, 25, 23, 45, 34, 39, 26, 19 prototype compounds were identified in serum, heart, liver, spleen, lung, kidney, brain, fat, and testicles, respectively. Meanwhile, an LC-MS based analytical method was established for simultaneous determination of chlorogenic acid, swertiamarin, caffeic acid, sweroside, liquiritin, prim-O-glucosylcimifugin, arctiin, 5-O-methylvisammioside and arctigenin in biological samples. The tissue distribution(serum, liver and lung) of these nine aim constituents in rats after oral administration of Jingyin Granules were investigated. It was found that these nine constituents could be quickly absorbed into circulation system and then distributed to liver and lung tissues. Except arctigenin, the exposure of other eight aim constituents to serum and lung was peaked at 1 h. At 1 h, the exposure of these components to lung tissue were ranked as follows: swertiamarin [(75 191.0±3 483.21) ng·g~(-1)]>arctiin [(2 716.5±36.06) ng·g~(-1)]>5-O-methylvisammioside [(585.1±0.71) ng·g~(-1)]>arctigenin [(437.45±3.18) ng·g~(-1)]>chlorogenic acid [(308.1±5.66) ng·g~(-1)]>prim-O-glucosylcimifugin [(211.35±2.19) ng·g~(-1)]>sweroside [(184.3±9.05) ng·g~(-1)]>caffeic acid [(175.95±2.05) ng·g~(-1)]>liquiritin [(174.78±153.34) ng·g~(-1)]. In summary, an UHPLC-Q-Exactive Orbitrap HR-MS method has been established for rapid and accurate identification of the constituents in Jingyin Granules, while the tissue distribution of nine major absorpted constituents were investigated in rats following oral administration of Jingyin Granules. These findings provided key information and guidance for further studies on pharmacodynamic substances and clinical applications of Jingyin Granules.
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http://dx.doi.org/10.19540/j.cnki.cjcmm.20200903.201DOI Listing
November 2020

Perovskite Films with Reduced Interfacial Strains via a Molecular-Level Flexible Interlayer for Photovoltaic Application.

Adv Mater 2020 Sep 9;32(38):e2001479. Epub 2020 Aug 9.

Institute of Functional Nano and Soft Materials (FUNSOM), Jiangsu Key Laboratory for Carbon-Based Functional Materials and Devices, Soochow University, Suzhou, 215123, China.

Interface strains and lattice distortion are inevitable issues during perovskite crystallization. Silane as a coupling agent is a popular connector to enhance the compatibility between inorganic and organic materials in semiconductor devices. Herein, a protonated amine silane coupling agent (PASCA-Br) interlayer between TiO and perovskite layers is adopted to directionally grasp both of them by forming the structural component of a lattice unit. The pillowy alkyl ammonium bromide terminals at the upper side of the interlayer provide well-matched growth sites for the perovskite, leading to mitigated interface strain and ensuing lattice distortion; meanwhile, its superior chemical compatibility presents an ideal effect on healing the under-coordinated Pb atoms and halogen vacancies of bare perovskite crystals. The PASCA-Br interlayer also serves as a mechanical buffer layer, inducing less cracked perovskite film when bending. The developed molecular-level flexible interlayer provides a promising interfacial engineering for perovskite solar cells and their flexible application.
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http://dx.doi.org/10.1002/adma.202001479DOI Listing
September 2020

["'s five-needle method" as the main treatment for allergic rhinitis and asthma syndrome: a multi-center randomized controlled trial].

Zhongguo Zhen Jiu 2020 May;40(5):483-7

College of Acupuncture-Moxibustion and Tuina, Henan University of CM, Zhengzhou 450008, China; Department of Acupuncture and Moxibustion, Third Affiliated Hospital of Henan University of CM, Zhengzhou 450008.

Objective: To compare the clinical effect differences between "'s five-needle method" and routine acupoint selection on allergic rhinitis and asthma syndrome.

Methods: A total of 210 patients with allergic rhinitis and asthma syndrome were randomly divided into an observation group (105 cases, 4 cases dropped off) and a control group (105 cases, 4 cases dropped off). The patients in the observation group were treated with "'s five-needling method", and the acupoints of Feishu (BL 13), Dazhui (GV 14), Fengmen (BL 12), Yintang (GV 29), Shangyingxiang (EX-HN 8) and Hegu (LI 4), etc. were selected; the patients in the control group was treated with routine acupuncture, and the acupoints of Feishu (BL 13), Zhongfu (LU 1), Taiyuan (LU 9), Dingchuan (EX-B 1), Danzhong (CV 17), Yintang (GV 29), Fengmen (BL 12) and Zusanli (ST 36), etc. were selected. The treatment in the two groups was given once a day, 6 times a week, for 4 weeks. The score of symptoms and signs was observed before and after treatment as well as 1 month, 2 months and 3 months after treatment. The forced expiratory volume in 1 second (FEV1), peak expiratory flow (PEF) and eosinophils in peripheral blood were measured before and after treatment in the two groups. After treatment, the clinical therapeutic effect was compared between the two groups.

Results: The total effective rate was 98.0% (99/101) in the observation group, which was superior to 94.1% (95/101) in the control group (<0.01). Compared before treatment, the total score of symptoms and signs in the two groups was significantly decreased at 1, 2, 3 and 4 weeks of treatment (<0.01); after treatment and at each time point of follow-up, the total score of symptoms and signs in the observation group was lower than that in the control group (<0.01). Compared with 4 weeks of treatment, the total score of symptoms and signs at each time point of follow-up was not statistically different in the observation group (>0.05), and the total score of symptoms and signs in the third month of follow-up in the control group was significantly increased (<0.05). After treatment, FEV1 and PEF in the two groups were increased (<0.01), eosinophil count in peripheral blood was decreased (<0.01), and the improvement in the observation group was greater than that in the control group (<0.01, <0.05).

Conclusion: "'s five-needle method" can improve the clinical symptoms and pulmonary function, reduce the count of eosinophils in peripheral blood in patients with allergic rhinitis and asthma syndrome, and the curative effect is better than routine acupuncture.
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http://dx.doi.org/10.13703/j.0255-2930.20190412-0007DOI Listing
May 2020

Mitochondrial aconitase controls adipogenesis through mediation of cellular ATP production.

FASEB J 2020 05 24;34(5):6688-6702. Epub 2020 Mar 24.

Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, China.

Mitochondrial aconitase (Aco2) catalyzes the conversion of citrate to isocitrate in the TCA cycle, which produces NADH and FADH2, driving synthesis of ATP through OXPHOS. In this study, to explore the relationship between adipogenesis and mitochondrial energy metabolism, we hypothesize that Aco2 may play a key role in the lipid synthesis. Here, we show that overexpression of Aco2 in 3T3-L1 cells significantly increased lipogenesis and adipogenesis, accompanied by elevated mitochondrial biogenesis and ATP production. However, when ATP is depleted by rotenone, an inhibitor of the respiratory chain, the promotive role of Aco2 in adipogenesis is abolished. In contrast to Aco2 overexpression, deficiency of Aco2 markedly reduced lipogenesis and adipogenesis, along with the decreased mitochondrial biogenesis and ATP production. Supplementation of isocitrate efficiently rescued the inhibitory effect of Aco2 deficiency. Similarly, the restorative effect of isocitrate was abolished in the presence of rotenone. Together, these results show that Aco2 sustains normal adipogenesis through mediating ATP production, revealing a potential mechanistic link between TCA cycle enzyme and lipid synthesis. Our work suggest that regulation of adipose tissue mitochondria function may be a potential way for combating abnormal adipogenesis related diseases such as obesity and lipodystrophy.
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http://dx.doi.org/10.1096/fj.201903224RRDOI Listing
May 2020

A Potential Nutraceutical Candidate Lactucin Inhibits Adipogenesis through Downregulation of JAK2/STAT3 Signaling Pathway-Mediated Mitotic Clonal Expansion.

Cells 2020 01 31;9(2). Epub 2020 Jan 31.

Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling 712100, China.

The prevalence of obesity has increased dramatically worldwide in the past ~50 years. Searching for safe and effective anti-obesity strategies are urgently needed. Lactucin, a plant-derived natural small molecule, is known for anti-malaria and anti-hyperalgesia. The study is to investigate whether lactucin plays a key role in adipogenesis. To this end, in vivo male C57BL/6 mice fed a high-fat diet (HFD) were treated with 20 mg/kg/day of lactucin or vehicle by gavage for seven weeks. Compared with vehicle-treated controls, Lactucin-treated mice showed lower body mass and mass of adipose tissue. Consistently, in vitro 3T3-L1 cells were treated with 20 μM of lactucin. Compared to controls, lactucin-treated cells showed significantly less lipid accumulation during adipocyte differentiation and lower levels of lipid synthesis markers. Mechanistically, we showed the anti-adipogenic property of lactucin was largely limited to the early stage of adipogenesis. Lactucin-treated cells fail to undergo mitotic clonal expansion (MCE). Further studies demonstrate that lactucin-induced MCE arrests might result from reduced phosphorylation of JAK2 and STAT3. We then asked whether activation of JAK2/STAT3 would restore the inhibitory effect of lactucin on adipogenesis with pharmacological STAT3 activator colivelin. Our results revealed similar levels of lipid accumulation between lactucin-treated cells and controls in the presence of colivelin, indicating that inactivation of STAT3 is the limiting factor for the anti-adipogenesis of lactucin in these cells. Together, our results provide the indication that lactucin exerts an anti-adipogenesis effect, which may open new therapeutic options for obesity.
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http://dx.doi.org/10.3390/cells9020331DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072480PMC
January 2020

Enhanced dehalogenation and coupled recovery of complex electronic display housing plastics by sub/supercritical CO.

J Hazard Mater 2020 01 3;382:121140. Epub 2019 Sep 3.

Department of Solid Waste Treatment and Recycling, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, 18 Shuangqing Road, Beijing, 100085, China; University of Chinese Academy of Sciences, Beijing, 100049, China.

Electronic display housing plastics contain a high amount of halogenated compounds such as brominated flame retardants (BFRs) and polyvinyl chloride (PVC). Compared with moderate critical conditions of conventional eco-friendly sub/supercritical carbon dioxide (Sc-CO), a novel and sustainable procedure by using improved Sc-CO was developed for disposal of this type of plastic. The main merit of the process was that complex halogen-containing plastics were safely disposed and halogen-free products were recycled without using catalysts or additives. It was discovered that additive BFRs were initially extracted by Sc-CO technique and then it decomposed accompanied with PVC rapidly to form HBr and HCl, which could be separated by traditional bromine stripping techniques from seawater. Based on response surface methodology (RSM), the maximum debromination and dechlorination efficiencies were achieved at 99.51% and 99.12% respectively. After the treatment, halogen-free products such as solid carbon materials and organic chemical feedstocks were obtained. Mechanism study elucidated that free radicals reaction involving chain initiation, growth and termination induced the polymer decomposition to form these products. This study provides an applicable and green approach for disposal and recovery of halogen-containing plastics.
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http://dx.doi.org/10.1016/j.jhazmat.2019.121140DOI Listing
January 2020

Polarized Ferroelectric Polymers for High-Performance Perovskite Solar Cells.

Adv Mater 2019 Jul 4;31(30):e1902222. Epub 2019 Jun 4.

Department of Materials Science and Engineering, University of California, Los Angeles, CA, 90095, USA.

In hybrid organic-inorganic lead halide perovskite solar cells, the energy loss is strongly associated with nonradiative recombination in the perovskite layer and at the cell interfaces. Here, a simple but effective strategy is developed to improve the cell performance of perovskite solar cells via the combination of internal doping by a ferroelectric polymer and external control by an electric field. A group of polarized ferroelectric (PFE) polymers are doped into the methylammonium lead iodide (MAPbI ) layer and/or inserted between the perovskite and the hole-transporting layers to enhance the build-in field (BIF), improve the crystallization of MAPbI , and regulate the nonradiative recombination in perovskite solar cells. The PFE polymer-doped MAPbI shows an orderly arrangement of MA cations, resulting in a preferred growth orientation of polycrystalline perovskite films with reduced trap states. In addition, the BIF is enhanced by the widened depletion region in the device. As an interfacial dipole layer, the PFE polymer plays a critical role in increasing the BIF. This combined effect leads to a substantial reduction in voltage loss of 0.14 V due to the efficient suppression of nonradiative recombination. Consequently, the resulting perovskite solar cells present a power conversion efficiency of 21.38% with a high open-circuit voltage of 1.14 V.
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http://dx.doi.org/10.1002/adma.201902222DOI Listing
July 2019

An Epistatic Interaction between and Reveals New Pathways of Adipose Tissue Lipolysis.

Cells 2019 04 29;8(5). Epub 2019 Apr 29.

Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling 712100, China.

White adipose tissue (WAT) lipolysis contributes to energy balance during fasting. Lipolysis can proceed by the sequential hydrolysis of triglycerides (TGs) by adipose triglyceride lipase (ATGL), then of diacylglycerols (DGs) by hormone-sensitive lipase (HSL). We showed that the combined genetic deficiency of ATGL and HSL in mouse adipose tissue produces a striking different phenotype from that of isolated ATGL deficiency, inconsistent with the linear model of lipolysis. We hypothesized that the mechanism might be functional redundancy between ATGL and HSL. To test this, the TG hydrolase activity of HSL was measured in WAT. HSL showed TG hydrolase activity. Then, to test ATGL for activity towards DGs, radiolabeled DGs were incubated with HSL-deficient lipid droplet fractions. The content of TG increased, suggesting DG-to-TG synthesis rather than DG hydrolysis. TG synthesis was abolished by a specific ATGL inhibitor, suggesting that ATGL functions as a transacylase when HSL is deficient, transferring an acyl group from one DG to another, forming a TG plus a monoglyceride (MG) that could be hydrolyzed by monoglyceride lipase. These results reveal a previously unknown physiological redundancy between ATGL and HSL, a mechanism for the epistatic interaction between and . It provides an alternative lipolytic pathway, potentially important in patients with deficient lipolysis.
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http://dx.doi.org/10.3390/cells8050395DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6563012PMC
April 2019

[The role of endoplasmic reticulum stress in pulmonary hypertension in rat induced by chronic hypoxia and hypercapnia].

Zhongguo Ying Yong Sheng Li Xue Za Zhi 2018 Apr;34(4):327-333

Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035.

Objective: To observe the pulmonary vascular remodeling in rats with pulmonary hypertension induced by hypoxia and hypercapnia, and to explore the role of endoplasmic reticulum stress in pulmonary hypertension.

Methods: Forty SD rats were random-ly divided into four groups:normoxic control group (N), hypoxia hypercapnia group (HH), ERS inhibitor 4-phenylbutyric acid group (4-PBA), endoplasmic reticulum stress (ERS) pathway agonist tunicamycin group (TM), ten rats in each group.The mean pulmona-ry artery pressure (mPAP), mean carotid artery pressure (mCAP) and right ventricular hypertrophy index of rats in each group were measured.Pulmonary artery smooth muscle cells were identified by immunofluorescence α-smooth muscle actin (α-SMA).Morphologi-cal changes of lung tissue and pulmonary artery were observed by electron microscope.The apoptotic index of pulmonary artery smooth muscle cells in each group was detected by TUNEL.Reverse transcription polymerase chain reaction (RT-PCR) and Western blot were used to detect the expression of glucose-regulated protein (GRP78), C/EBP homologous protein (CHOP), c-Jun N-terminal kinase (JNK) and cysteinyl aspartate specific proteinase-12 (caspase-12) mRNA and protein in each group.

Results: ①Compared with the N group, the mPAP, the ratio of right ventricle weight to left ventricle plus ventricular septum weight[RV/(LV+S)]and the ratio of pulmonary artery wall area to total tube area (WA/TA) were increased (<0.01), and the ratio of pulmonary artery luminal area to total tube area (LA/TA) were decreased (<0.01), pulmonary artery smooth muscle cell apoptosis index were decreased (<0.05 or <0.01) in HH group, 4-PBA group and TM group.ERS related protein and mRNA expressions were increased, the differences were statistically significant.②Compared with the HH group, the mPAP, [RV/(LV+S)]and WA/TA of 4-PBA group were decreased ( <0.01), LA/TA and pulmonary artery smooth muscle cell apoptosis index were increased (<0.01, <0.05).The expressions of ERS related protein and mRNA were all decreased (<0.05 or <0.01).③Compared with the HH group, the mPAP, [RV/(LV+S)]and WA/TA of TM group were increased (<0.05 or <0.01), pulmonary artery middle layer thickened, LA/TA and pulmonary artery smooth muscle cell apoptotic index were decreased (<0.01).ERS related protein and mRNA expressions were increased with statistical significance except GRP78 protein.

Conclusions: Pulmonary vascular remodeling in rats with pulmonary hypertension induced by hypoxia and hypercapnia may be related to the excessive proliferation of pulmonary artery smooth muscle cells and too little apopto-sis;ERS related factors (JNK, caspase-12 and CHOP) are involved in the regulation of pulmonary hypertension induced by hypoxia hypercapnia.
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http://dx.doi.org/10.12047/j.cjap.5644.2018.075DOI Listing
April 2018

[The effect of Yiqi Wenyang Huoxue Huatan Fang on hypoxia-hypercarbia induced pulmonary hypertension and its mechanism].

Zhongguo Ying Yong Sheng Li Xue Za Zhi 2018 May;34(5):408-413

Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035, China.

Objective: To investigate the effect of Yiqi Wenyang Huoxue Huatan Fang (YWHHF) on alleviating hypoxia-hypercarbia pulmonary hypertension by inhibiting endothelial-mesenchymal transition (EndoMT) BMP-7/Smads pathway.

Methods: Fifty male healthy SD rats of clean grede, weighting (180~220) g, were randomly divided into 5 groups (=10):normoxia group (N), hypoxia-hypercarbia group (HH); YWHHF high dose group (YH), middle dose group (YM) and low dose group (YL). The rats in N group were kept in normal oxygen environment, the remaining four groups were intermittently exposed to hypoxia-hypercarbia environment (9%~11% O, 5%~6% CO) for 4 weeks, 6 days a week, 8 hours per day. The rats in YH, YM, YL groups were received YWHHF gavage in a dosageof 0.6, 0.3, 0.15g/kg respectively (3 ml/kg),the rats in N and HH groups were received equal volume of normal saline. After 4 weeks, the mean pulmonary arterial pressure(mPAP) was detected,the right ventricular free wall and left ventricle plus ventricular septum were isolated to determine the right ventricular hypertrophy index. Lung ultrastructural changes were surveyed under an electronic microscopy, the changes of pulmonary artery structure surveyed by immunofluorescence, the mRNA levels of alpha-smooth muscle actin (α-SMA)、platelet endothelial cell adhesion molecule-1 (CD31)、bone morphogenetic protein-7 (BMP-7)、drosophila mothers against decapentaplegic protein1/5/8 (Smad1/5/8) were detected by RT-PCR, and the protein levels of α-SMA、CD31、BMP-7、p-Smad1/5/8 and Smad1/5/8 were detected by Western blot.

Results: Compared with N group, mPAP and the right ventricular hypertrophy index were increased,some significant injuries also were discovered under microscopic observation,the mRNA and protein expression of α-SMA was increased, and the mRNA expressions of CD31、BMP-7、Smad1/5/8 were decreased in the other four groups, the protein expressions of CD31、BMP-7、p-Smad1/5/8 were decreased(<0.05). Compared with HH group, the above changes in YH、YM、YL groups were all improved (<0.05).

Conclusions: YWHHF can inhibit EndoMT to alleviate pulmonary hypertension, and the mechanism may be related to the promotion of the expression of BMP-7/Smads pathway.
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http://dx.doi.org/10.12047/j.cjap.5626.2018.093DOI Listing
May 2018

Theory of Chiral p-Wave Superconductivity with Near Nodes for Sr_{2}RuO_{4}.

Phys Rev Lett 2019 Jan;122(2):027002

National Laboratory of Solid State Microstructures & School of Physics, Nanjing University, Nanjing 210093, China.

We use the functional renormalization group method to study a three-orbital model for superconducting Sr_{2}RuO_{4}. Although the pairing symmetry is found to be a chiral p wave, the atomic spin-orbit coupling induces near nodes for quasiparticle excitations. Our theory explains a major experimental puzzle between a d-wavelike feature observed in thermal experiments and the chiral p-wave triplet pairing revealed in nuclear-magnetic resonance and the Kerr effect.
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http://dx.doi.org/10.1103/PhysRevLett.122.027002DOI Listing
January 2019

Atorvastatin protects BV‑2 mouse microglia and hippocampal neurons against oxygen‑glucose deprivation‑induced neuronal inflammatory injury by suppressing the TLR4/TRAF6/NF‑κB pathway.

Mol Med Rep 2018 Jul 23;18(1):1058-1066. Epub 2018 May 23.

Department of Neurology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, Sichuan 610072, P.R. China.

Atorvastatin is a member of the statin class of drugs, which competitively inhibit the activity of 5‑hydroxy‑3‑methylglutaryl‑coenzyme A reductase. The aim of the present study was to assess whether atorvastatin may protect BV‑2 microglia and hippocampal neurons against oxygen‑glucose deprivation (OGD)‑induced neuronal inflammatory injury and to determine the underlying mechanisms by which its effects are produced. Cell viability and apoptotic ability were assessed using an MTT assay and annexin V‑fluorescein isothiocyanate/propidium iodide double staining followed by flow cytometry, respectively. The expression of inflammation and apoptosis‑associated mRNAs and proteins were assessed using reverse transcription‑quantitative polymerase chain reaction and western blotting, and the expression of inflammatory factors was determined using ELISA. The results of the current study revealed that atorvastatin treatment suppressed the viability of OGD BV‑2 microglia and hippocampal neurons. Furthermore, atorvastatin treatment reduced the expression of proinflammatory factors in OGD BV‑2 microglia. Additionally, it was demonstrated to downregulate the toll‑like receptor 4 (TLR4)/tumor necrosis factor receptor‑associated factor 6 (TRAF6)/nuclear factor‑κB (NF‑κB) pathway in OGD BV‑2 microglia. Atorvastatin also inhibited the apoptosis of OGD hippocampal neurons by regulating the expression of apoptosis‑associated proteins. It was concluded that atorvastatin treatment may protect BV‑2 microglia and hippocampal neurons from OGD‑induced neuronal inflammatory injury by suppressing the TLR4/TRAF6/NF‑κB pathway. This may provide a potential strategy for the treatment of neuronal injury.
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http://dx.doi.org/10.3892/mmr.2018.9055DOI Listing
July 2018

Complement 5a stimulates macrophage polarization and contributes to tumor metastases of colon cancer.

Exp Cell Res 2018 05 15;366(2):127-138. Epub 2018 Mar 15.

Beijing Anzhen Hospital Affiliated to the Capital Medical University, Beijing 100029, China; The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Capital Medical University, Ministry of Education, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing collaborative innovative research center for cardiovascular diseases, Beijing 100029, China. Electronic address:

Inflammatory cells such as macrophages can play a pro-tumorigenic role in the tumor stroma. Tumor-associated macrophages (TAMs) generally display an M2 phenotype with tumor-promoting activity; however, the mechanisms regulating the TAM phenotype remain unclear. Complement 5a (C5a) is a cytokine-like polypeptide that is generated during complement system activation and is known to promote tumor growth. Herein, we investigated the role of C5a on macrophage polarization in colon cancer metastasis in mice. We found that deficiency of the C5a receptor (C5aR) severely impairs the metastatic ability of implanted colon cancer cells. C5aR was expressed on TAMs, which exhibited an M2-like functional profile in colon cancer liver metastatic lesions. Furthermore, C5a mediated macrophage polarization and this process relied substantially on activation of the nuclear factor-kappa B (NF-κB) pathway. Finally, analysis of human colon carcinoma indicated that C5aR expression is negatively associated with tumor differentiation grade. Our results demonstrate that C5aR has a central role in regulating the M2 phenotype of TAMs, which in turn, contributes to hepatic metastasis of colon cancer through NF-κB signaling. C5a is a potential novel marker for cancer prognosis and drugs targeting complement system activation, specifically the C5aR pathway, may offer new therapeutic opportunities for colon cancer management.
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http://dx.doi.org/10.1016/j.yexcr.2018.03.009DOI Listing
May 2018

IL-18 cleavage triggers cardiac inflammation and fibrosis upon β-adrenergic insult.

Eur Heart J 2018 01;39(1):60-69

Institute of Vascular Medicine, Cardiology Department, Peking University Third Hospital, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptide, Ministry of Health, and Beijing Key Laboratory of Cardiovascular Receptors Research, No. 49, Huayuan Bei Road, Haidian District, Beijing 100191, China.

Aims: Rapid over-activation of β-adrenergic receptor (β-AR) upon stress leads to cardiac inflammation, a prevailing factor that underlies heart injury. However, mechanisms by which acute β-AR stimulation induce cardiac inflammation still remain unknown. Here, we set out to identify the crucial role of inflammasome/interleukin (IL)-18 in initiating and maintaining cardiac inflammatory cascades upon β-AR insult.

Methods And Results: Male C57BL/6 mice were injected with a single dose of β-AR agonist, isoproterenol (ISO, 5 mg/kg body weight) or saline subcutaneously. Cytokine array profiling demonstrated that chemokines dominated the initial cytokines upregulation specifically within the heart upon β-AR insult, which promoted early macrophage infiltration. Further investigation revealed that the rapid inflammasome-dependent activation of IL-18, but not IL-1β, was the critical up-stream regulator for elevated chemokine expression in the myocardium upon ISO induced β1-AR-ROS signalling. Indeed, a positive correlation was observed between the serum levels of norepinephrine and IL-18 in patients with chest pain. Genetic deletion of IL-18 or the up-stream inflammasome component NLRP3 significantly attenuated ISO-induced chemokine expression and macrophage infiltration. In addition, IL-18 neutralizing antibodies selectively abated ISO-induced chemokines, proinflammatory cytokines and adhesion molecules but not growth factors. Moreover, blocking IL-18 early after ISO treatment effectively attenuated cardiac inflammation and fibrosis.

Conclusion: Inflammasome-dependent activation of IL-18 within the myocardium upon acute β-AR over-activation triggers cytokine cascades, macrophage infiltration and pathological cardiac remodelling. Blocking IL-18 at the early stage of β-AR insult can successfully prevent inflammatory responses and cardiac injuries.
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http://dx.doi.org/10.1093/eurheartj/ehx261DOI Listing
January 2018

Recycling of spent lithium-ion battery with polyvinyl chloride by mechanochemical process.

Waste Manag 2017 Sep 30;67:232-239. Epub 2017 May 30.

Department of Solid Waste Treatment and Recycling, Research Center for Eco-environmental Sciences, Chinese Academy of Sciences, 18 Shuangqing Road, Beijing 100085, China; University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address:

In the present study, cathode materials (C/LiCoO) of spent lithium-ion batteries (LIBs) and waste polyvinyl chloride (PVC) were co-processed via an innovative mechanochemical method, i.e. LiCoO/PVC/Fe was co-grinded followed by water-leaching. This procedure generated recoverable LiCl from Li by the dechlorination of PVC and also generated magnetic CoFeO from Co. The effects of different additives (e.g. alkali metals, non-metal oxides, and zero-valent metals) on (i) the conversion rates of Li and Co and (ii) the dechlorination rate of PVC were investigated, and the reaction mechanisms were explored. It was found that the chlorine atoms in PVC were mechanochemically transformed into chloride ions that bound to the Li in LiCoO to form LiCl. This resulted in reorganization of the Co and Fe crystals to form the magnetic material CoFeO. This study provides a more environmentally-friendly, economical, and straightforward approach for the recycling of spent LIBs and waste PVC compared to traditional processes.
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http://dx.doi.org/10.1016/j.wasman.2017.05.013DOI Listing
September 2017

[The regulation of MAPK signaling pathway on cell proliferation and apoptosis in hypoxic PASMCs of rats].

Zhongguo Ying Yong Sheng Li Xue Za Zhi 2017 Mar;33(3):226-230

Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035, China.

Objective: To explore the relationship between hypoxic pulmonary arterial smooth muscle cells(PASMCs)proliferation, apop-tosis and mitogen-activated protein kinases(MAPK) signal pathway in rats.

Methods: PASMCs were obtained from male SD rats by the enzyme digestion method and primarily cultured; PASMCs were identified through two methods:immunofluorescence staining and light microscopy; the 4~6th generation PASMCs of logarithmic growth state of good growth period were selected, and randomly divided into 7 groups:normoxic con-trol group (N), hypoxia group (H), DMSO group (D), extracellular signal-regulated kinase1/2(ERK1/2) inhibitor-U0126 group (U) and p38MAPK inhibitor-SB203580 group (S), the p38MAPK activator-Anisomycin group (A), the ERK1/2 activator-Staurosporine Aglycone group (SA). When all the models were completed, the all groups joined the CCK-8 to measure cell proliferation; cell apoptosis of each group was detected by TUNEL kit after the modeling.

Results: Compared with N group, the expression of OD value in H group was up-regulated (0.990 ±0.041 1.143 ±0.033, < 0.01). There was no statistical significance on PASMCs apoptosis index(AI) in H group (4.913 ±0.451 5.452 ±0.557, > 0.05); Compared With H group, there were no statistical significance on the expression of PASMCs OD value and apoptosis index(AI)in D group (1.143 ±0.033 1.142 ±0.049,5.452 ±0.557 5.402 ±0.651, > 0.05); the expression of OD value in U group was down-regulated, and the expression of AI was up-regulated (1.143 ±0.033 0.985 ±0.078, 5.452 ±0.557 10.145 ±2.545, < 0.01); the expression of OD value in S group was up-regulated, and the expression of AI was down-regulated (1.143 ±0.033 1.295 ±0.039, 5.452 ±0.557 3.093 ±0.409, < 0.01); the expression of OD value in A group was down-regulated, and the expres-sion of AI was up-regulated (1.143 ±0.033 0.347 ±0.067, 5.452 ±0.557 25.753 ±1.262, < 0.01); the expression of OD value in SA group was up-regulated, and the expression of AI was down-regulated (1.143 ±0.033 1.685 ±0.100, 5.452 ±0.557 1.700 ±0.095, < 0.01).

Conclusions: The regulation of PASMCs' proliferation and apoptosis under hypoxia condition have a relationship with the participation of MAPK signal pathway.
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http://dx.doi.org/10.12047/j.cjap.5422.2017.056DOI Listing
March 2017

[Role of TRPC6 in pulmonary artery smooth muscle cells proliferation and apoptosis under hypoxia and hypercapnia].

Sheng Li Xue Bao 2017 Feb;69(1):47-54

Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035, China.

The present study was to investigate the role of TRPC6 in pulmonary artery smooth muscle cells (PASMCs) proliferation and apoptosis under hypoxia and hypercapnia. PASMCs were isolated from chloral hydrate-anesthetized male Sprague-Dawley (SD) rats. Cellular purity was assessed by immunofluorescence staining for smooth muscle α-actin under fluorescence microscopy. Passage 4-6 PASMCs were starved for 24 h in serum-free DMEM and divided into 5 groups randomly: normoxia, hypoxia and hypercapnia, DMSO, TRPC6 inhibitor SKF-96365 and TRPC6 activator OAG groups. The normoxic group was incubated under normoxia (5% CO, 21% O, 37 °C) for 24 h, and the others were incubated with corresponding drugs under hypoxic and hypercapnic (6% CO, 5% O, 37 °C) atmosphere for 24 h. TRPC6 mRNA was detected by reverse transcription-PCR. TRPC6 protein was detected by Western blotting. The proliferation of PASMCs was performed by CCK-8 kit. Apoptosis of the PASMCs was detected using TUNEL assay. The [Ca] in the PASMCs was measured using Fura 2-AM fluorescence. The results showed that the expressions of TRPC6 mRNA and protein, and [Ca] were upregulated under hypoxic and hypercapnic conditions. Hypoxia and hypercapnia promoted cellular proliferation and inhibited apoptosis in the PASMCs. OAG enhanced the above-mentioned effects of hypoxia and hypercapnia, whereas SKF-96365 reversed these effects. These results suggest that TRPC6 may play a role in PASMCs proliferation and apoptosis under hypoxia and hypercapnia by regulating [Ca].
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February 2017

[The effects of ERK1/2 pathway on the expression of calcium activated chloride channel in hypoxia in PASMCs rat model].

Zhongguo Ying Yong Sheng Li Xue Za Zhi 2017 Jan;33(1):47-50

Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035.

Objective: To investigate the expression of mRNA and protein of Calcium activated chloride channel (CLCA2) in hypoxic pulmonary artery smooth muscle cell (PASMCs) of rat and it's relationship with ERK1/2 signal pathway.

Methods: PASMCs were randomly divided into 5 groups including normal group(N group), hypoxia group(H group), DMSO group(D group), U0126 group (U group) and Staurosporine aglycone group(SA group). The protein expression of CLCA2 in PASMCs was detected by Western blot.The mRNA expression of CLCA2 was detected by half quantitative reverse transcription polymerase chain reaction (RT-PCR).

Results: The mRNA and protein expressions of CLCA2 in H group were significantly higher than N group (<0.01). Comparing with D group,the mRNA and protein expressions of CLCA2 were significantly increased in U group (<0.01),the mRNA expression of CLCA2 in SA group was obviously decreased (<0.01) with slightly decreasing of its protein expression.

Conclusions: Hypoxia promotes the expressions of mRNA and protein of CLCA2 in rat PASMCs. The ERK1/2 pathway activator Staurosporine aglycone reduces the mRNA and protein expression of CLCA2 in rats PASMCs and the ERK1/2 pathway inhibitor U0126 induces the upregulation of the mRNA and protein expressiosn of CLCA2 in rats PASMCs.
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http://dx.doi.org/10.12047/j.cjap.5448.2017.011DOI Listing
January 2017

[The effects and mechanisms of ligustrazine injection on pulmonary arterial hypertension in COPD patients].

Zhongguo Ying Yong Sheng Li Xue Za Zhi 2016 May;32(5):408-412

Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035.

Objective: To observe the effects of ligustrazine hydrochloride injection(LHI) on pulmonary arterial hypertension in chronic obstructive pulmonary disease(COPD) patients and to investigate its possible mechanisms.

Methods: Twenty-two cases of patients with COPD were randomly divided into conventional treatmentgroup (group C) and ligustrazine treatment group(group L), 11 persons were randomly selected from healthy subjects without lung disease served as normal control group(group N). Group C was given bed rest, low flow oxygen inhalation, bronchial diastolic agent, glucocorticoid and antibiotics and other conventional treatment, and group L was added with ligustrazine hydrochloride injection on the above mentioned basis treatment, group N was given no treatment. After 2 weeks, lung function, blood gas analysis and pulmonary arterial pressure were compared among the three groups, and the content of HS in plasma was tested with sensitive sulfur electrode method.

Results: ①After two weeks treatment, in group L and group C pulmonary function, blood gas analysis, pulmonary artery pressure were obviously improved, and group L was better than group C (<0.05); ② In group L the content of HS was increased (<0.01), group C had no significant difference (>0.05), and there was a significant difference between the two groups (<0.01).

Conclusions: Combination with LHI can effectively improve lung function. LHI mayrelieve hypoxic hypercapnia pulmonary hypertension induced by COPD through raising the content of HS.
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http://dx.doi.org/10.13459/j.cnki.cjap.2016.05.006DOI Listing
May 2016

[Dexmedetomidine prevents inflammatory responses in injured rat lung tissues induced by ischemia/reperfusion through inhibition of TLR4 expression].

Zhongguo Ying Yong Sheng Li Xue Za Zhi 2016 Apr;32(4):356-360

Ischemia/Reperfusion Injury Research Institute, Whenzhou Medical University, Whenzhou 325035.

Objective: To investigate the effect of Dexmedetomidine (Dex) on Toll-like receptor 4(TLR4) expression in lung during lung ischemia/reperfusion(I/R) in rats and its possible protecting mechanisms.

Methods: In vivo I/R model in left lung of SD rats was estab-lished. Fifty adult healthy male SD rats were randomly divided into five groups (=10):control group (Sham group), I/R group, Dex group, atipamezole group (Atip group) and Dex+Atip group. After the I/R experiment,rats were killed and the left lung tissues were harvest-ed to get the lung wet/dry weight(W/D); Ultrastructure of lung tissue were observed under light microscopy; The mRNA expression of TLR4 in lung tissues were determined by RT-PCR; The protein level of TLR4 in lung tissues was detected by Western blot.

Results: ①Compared with those in the Sham group, W/D and total lung water content (TLW) in other groups increased significantly (<0.05), the mRNA and protein expression levels of TLR4 in lung tissues increased too. The structure damages of lung tissues observed under light microscopy in other groups were more than that of Sham group. ②Compared with those in the I/R group, W/D and TLW in the Dex group were lower (<0.05, <0.01), the mRNA and protein expression levels of TLR4 in lung tissues decreased (<0.01), and reduced structure damages of lung tissues were observed under light microscopy in Dex group. ③Compared with those in the Dex group, W/D and TLW in the Dex+Atip group were higher (<0.01), the mRNA and protein expression levels of TLR4 in lung tissues increased (<0.01), and the structure damages of lung tissues observed under light microscopy were more serious. There was no significant difference of the above parameters among I/R、Atip、Dex+Atip groups.

Conclusions: Lung ischemia/reperfusion caused high expression of TLR4 and finally induced damages of the lung. Dexmedetomidine could inhibit TLR4 expression and alleviate the lung ischemia/reperfusion injury, which was related to activation of α2-adreno receptor.
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http://dx.doi.org/10.13459/j.cnki.cjap.2016.04.018DOI Listing
April 2016

An environmental benign process for cobalt and lithium recovery from spent lithium-ion batteries by mechanochemical approach.

Waste Manag 2016 May 7;51:239-244. Epub 2016 Mar 7.

Research Center for Eco-environmental Sciences, Chinese Academy of Sciences, 18 Shuangqing Road, Beijing 100085, China. Electronic address:

In the current study, an environmental benign process namely mechanochemical approach was developed for cobalt and lithium recovery from spent lithium-ion batteries (LIBs). The main merit of the process was that neither corrosive acid nor strong oxidant was applied. In the proposed process, lithium cobalt oxide (obtained from spent LIBs) was firstly co-grinded with various additives in a hermetic ball milling system, then Co and Li could be easily recovered by a water leaching procedure. It was found that EDTA was the most suitable co-grinding reagent, and 98% of Co and 99% of Li were respectively recovered under optimum conditions: LiCoO2 to EDTA mass ratio 1:4, milling time 4h, rotary speed 600r/min and ball-to-powder mass ratio 80:1, respectively. Mechanisms study implied that lone pair electrons provided by two nitrogen atoms and four hydroxyl oxygen atoms of EDTA could enter the empty orbit of Co and Li by solid-solid reaction, thus forming stable and water-soluble metal chelates Li-EDTA and Co-EDTA. Moreover, the separation of Co and Li could be achieved through a chemical precipitation approach. This study provides a high efficiency and environmentally friendly process for Co and Li recovery from spent LIBs.
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http://dx.doi.org/10.1016/j.wasman.2016.03.006DOI Listing
May 2016

MicroRNA Let-7i negatively regulates cardiac inflammation and fibrosis.

Hypertension 2015 Oct 10;66(4):776-85. Epub 2015 Aug 10.

From the Department of Pathology and Pathophysiology, School of Basic Medical Sciences (X.W., H.-X.W., C.-Y.Z., H.-H.L.) and Beijing AnZhen Hospital, The Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education, Beijing Institute of Heart Lung and Blood Vessel Diseases (Y.-L.L., C.-C.Z., J.D., H.-H.L.), Capital Medical University, Beijing, China; and Department of Cardiology, Institute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China (L.W., Y.-L.X.).

Angiotensin II stimulates fibroblast proliferation and substantially alters gene expression patterns leading to cardiac remodeling, but the mechanisms for such differences are unknown. MicroRNAs are a novel mechanism for gene expression regulation. Herein, we tested the miRNA and mRNA expression patterns in mouse heart using microarray assay and investigated their role in angiotensin II-induced cardiac remodeling. We found that let-7i was dynamically downregulated in angiotensin II-infused heart at day 3 and 7 and had the most targets that were mainly associated with cardiac inflammation and fibrosis. Overexpression or knockdown of let-7i in cultured cardiac fibroblasts demonstrated that let-7i played an inhibitory effect on the expression of its targets interleukin-6 and collagens. Furthermore, delivery of let-7i to mouse significantly inhibited angiotensin II-induced cardiac inflammation and fibrosis in a dose-dependent manner. Conversely, knockdown of let-7i aggravated this effect. Together, our results clearly demonstrate that let-7i acts as a novel negative regulator of angiotensin II-induced cardiac inflammation and fibrosis by suppressing the expression of interleukin-6 and multiple collagens in the heart and may represent a new potential therapeutic target for treating hypertensive cardiac fibrosis.
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http://dx.doi.org/10.1161/HYPERTENSIONAHA.115.05548DOI Listing
October 2015

[Effect of zige lyophilized powder for injection in improving acute cerebral microcirculation disturbance in rats].

Zhongguo Zhong Yao Za Zhi 2014 Feb;39(4):733-7

Objective: To investigate the effect of Zige lyophilized powder for injection in improving the acute cerebral microcirculation disturbance in rats.

Method: Window craniotomy was performed for rats after the drug administration for 14 days. The experimental microcirculation disturbance model was duplicated with high molecule dextran. After the drug administration, the micro-vein diameters of cerebral pla mater of various groups were observed and recorded under the biological microscope. The blood flow volume was monitored by laser Doppler flow-meter. HCT was measured by the electric resistance method. The hemorheological indexes were detected by the auto-hemorheological instrument.

Result: Zige lyophilized powder for injection (16.40, 32.70, 65.40 mg x kg(-1)) could significantly expand the micro-vein diameter of cerebral pla mater, improve the downward trend of the blood flow volume, and reduce the various hemorheological indexes.

Conclusion: Zige lyophilized powder for injection shows the effect in improving the cerebral microcirculation.
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February 2014

Cross talk between vascular smooth muscle cells and monocytes through interleukin-1β/interleukin-18 signaling promotes vein graft thickening.

Arterioscler Thromb Vasc Biol 2014 Sep 10;34(9):2001-11. Epub 2014 Jul 10.

From the Beijing An Zhen Hospital Affiliated the Capital Medical University, Department of Vascular Biology, Institute of Heart Lung and Blood Vessel Diseases, Beijing, China (P.L., Y.-l.L., Y.-n.W., C.-c.Z., X.A., C.-x.W., H.-t.S., J.D.); National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China (Z.-y.L.), National Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences, Beijing, China (M.-z.H., B.X.); and Department of Medicine, Baylor College of Medicine, Houston, TX (M.A.).

Objective: Interleukin (IL)-1β and IL-18 are key proinflammatory cytokines that play important roles in the pathophysiology of vein graft remodeling. However, the mechanism of IL-1β/IL-18 production and its role in the development of graft remodeling remain unclear.

Approach And Results: IL-1β/IL-18 were rapidly expressed in venous interposition grafts. Vascular smooth muscle cell (VSMC) death and monocytic inflammasome activation occurred in grafted veins. Necrotic VSMCs induced the expression of IL-1β, IL-18, and other inflammasome-associated proteins in monocytes, which was partially inhibited by their antagonist, recombinant IL-1ra-Fc-IL-18bp. Activated monocytes stimulated proliferation of VSMCs by activating cell growth-related signaling molecules (AKT, STAT3, ERK1/2, and mTOR [AKT/protein kinase B, signal transducer and activator of transcription 3, extracellular signal-regulated kinase 1/2, mammalian target of rapamycin]) and increasing production of platelet-derived growth factor-bb; these effects were suppressed by IL-1ra-Fc-IL-18bp. Activated monocytes also promoted migration of VSMCs, which was independent of IL-1β/IL-18 signaling. Importantly, administration of IL-1ra-Fc-IL-18bp inhibited activation of cell growth-related signaling molecules, VSMC proliferation, and vein graft thickening in vivo.

Conclusions: Our work identified an interaction among necrotic VSMCs, monocytes, and viable VSMCs through IL-1β/IL-18 signaling, which might be exploited as a therapeutic target in vein graft remodeling.
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http://dx.doi.org/10.1161/ATVBAHA.113.303145DOI Listing
September 2014

[Application of high-content screening and flow cytometry analysis techniques to evaluation of myocardial fibroblasts proliferation].

Sheng Li Xue Bao 2014 Apr;66(2):215-22

The Key laboratory of Remodeling Related Cardiovascular Diseases, Ministry of Education, Capital Medical University Affiliated Beijing Anzhen Hospital, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing 100029, China.

The proliferation of cardiac fibroblasts (CFs) is a key pathological process in the cardiac remodeling. To establish an objective, quantitative method for the analysis of cell proliferation and cell cycle, we applied the high-content screening (HCS) and flow cytometry (FCM) techniques. CFs, isolated by enzyme digestion from newborn C57BL/6J mice, were serum starved for 12 h and then given 10% fetal bovine serum (FBS) for 24 h. Followed by BrdU and DAPI (or 7-AAD) staining, CFs proliferation and cell cycle were analyzed by HCS and FCM, respectively. Discoidin domain receptor 2 (DDR2) staining indicated that the purity of isolated CFs was over 95%. (1) HCS analysis showed that the ratio of BrdU-positive cells was significantly increased in 10% FBS treated group compared with that in serum-free control group [(12.96 ± 0.67)% vs (2.77 ± 0.33)%; P < 0.05]. Cell cycle analysis showed that CFs in G0/G1 phase were diploid, and CFs in S phase were companied with proliferation, DNA replication and enlarged nuclei; CFs in G2 phase were tetraploid, and CFs in M phase produced two identical cells (2N). (2) FCM analysis showed that the ratio of BrdU-positive cells was increased in 10% FBS treated group compared with that in the control group [(11.10 ± 0.42)% vs (2.22 ± 0.31)%; P < 0.05]; DNA content histogram of cell cycle analysis indicated that the platform of S phase elevated in 10% FBS group compared with control group. (3) There were no differences between the two methods in the results of proliferation and cell cycle analysis. In conclusion, HCS and FCM methods are reliable, stable and consistent in assessment of the proliferation and cell cycle in CFs.
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April 2014

Effect of Morinda officinalis capsule on osteoporosis in ovariectomized rats.

Chin J Nat Med 2014 Mar;12(3):204-12

College of Pharmaceutical Sciences, Institute of Chinese Medicine, Pharmacology of Chinese Materia Medica-the key constructing discipline by the State Administrative Bureau of TCM, Southwest University, Chongqing 400715, China. Electronic address:

Aim: To explore the therapeutic effects of Morinda officinalis capsules (MOP) on osteoporosis in ovariectomized rats.

Methods: Six-month-old female Sprague-Dawley rats were induced for postmenopausal osteoporosis (PMOP) by bilateral ovariectomy and divided into seven groups as follows: sham-operated group, ovariectomized (OVX) control group, OVX treated with xianlinggubao (XLGB) (270 mg·kg⁻¹·d⁻¹), OVX treated with alendronate sodium (ALN) (3 mg·kg⁻¹·d⁻¹), and OVX treated with Morinda officinalis capsule (MOP) of graded doses (90, 270 and 810 mg·kg⁻¹·d⁻¹) groups. Oral treatments were administered daily on the 4(th) week after ovariectomy and lasted for 12 weeks. The bone mineral density was evaluated by dual-energy X-ray absorptiometry. The tartrate-resistant acid phosphatase (TRAP), alkaline phosphatase (AKP), and osteocalcin (OC) levels in the serum and plasma were determined by standard colorimetric and enzyme immunoassays methods. Bone biomechanical properties and morphological parameters were analyzed by three-point bending test and histomorphometry respectively.

Results: Morinda officinalis capsules at all doses were able to significantly prevent the OVX-induced loss of bone mass due to diminishing serum AKP and TRAP levels while elevating OC level in the plasma. Morinda officinalis capsules also enhanced the bone strength and prevented the deterioration of trabecular microarchitecture.

Conclusion: Morinda officinalis capsules possess potent anti-osteoporotic activity in OVX rats which could be an effective treatment for postmenopausal osteoporosis.
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http://dx.doi.org/10.1016/S1875-5364(14)60034-0DOI Listing
March 2014
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