Publications by authors named "Lingqun Zhu"

27 Publications

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The role of S-nitrosylation of PFKM in regulation of glycolysis in ovarian cancer cells.

Cell Death Dis 2021 04 15;12(4):408. Epub 2021 Apr 15.

Cancer Research Institute, Guangdong Provincial Key Laboratory of Cancer Immunotherapy, Guangzhou Key Laboratory of Tumor Immunology Research, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.

One of the malignant transformation hallmarks is metabolism reprogramming, which plays a critical role in the biosynthetic needs of unchecked proliferation, abrogating cell death programs, and immunologic escape. However, the mechanism of the metabolic switch is not fully understood. Here, we found that the S-nitrosoproteomic profile of endogenous nitrogen oxide in ovarian cancer cells targeted multiple components in metabolism processes. Phosphofructokinase (PFKM), one of the most important regulatory enzymes of glycolysis, was S-nitrosylated by nitric oxide synthase NOS1 at Cys351. S-nitrosylation at Cys351 stabilized the tetramer of PFKM, leading to resist negative feedback of downstream metabolic intermediates. The PFKM-C351S mutation decreased the proliferation rate of cultured cancer cells, and reduced tumor growth and metastasis in the mouse xenograft model. These findings indicated that S-nitrosylation at Cys351 of PFKM by NOS1 contributes to the metabolic reprogramming of ovarian cancer cells, highlighting a critical role of endogenous nitrogen oxide on metabolism regulations in tumor progression.
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http://dx.doi.org/10.1038/s41419-021-03681-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8050300PMC
April 2021

A meta-analysis of the clinical efficacy of Tanreqing injection combined with antibiotics vs antibiotics alone for treating pulmonary infection secondary to intracerebral hemorrhage.

Medicine (Baltimore) 2021 Mar;100(11):e24905

Key Laboratory of Chinese Internal Medicine of Educational Ministry and Beijing, Dongzhimen Hospital.

Background: Pulmonary infection is the most common complication to develop after intracerebral hemorrhage (ICH). Antibiotics have certain limitations when used to treat pulmonary infection, while Tanreqing injection (TRQI) is extensively used to treat pulmonary infection as an adjuvant to antibiotics. The aim of this meta-analysis was to investigate the clinical efficacy of TRQI for the treatment of lung infection secondary to ICH.

Methods: Randomized controlled trials (RCTs) assessing the combination of TRQI and antibiotics compared to antibiotics alone for pulmonary infection after ICH were comprehensively searched for in 7 electronic databases from their establishment to August 2020. Two independent researchers conducted the literature retrieval, screening, and data extraction. The assessment tool of Cochrane risk of bias and Review Manager 5.3 software were applied to assess the methodological quality and analyze the data, respectively.

Results: Seventeen RCTs involving 1122 patients with pulmonary infection after ICH were included. Compared to antibiotics alone, the combination treatment enhanced the clinical effective rate, shortened the hospital stay, reduced the white blood cell, procalcitonin, and C-reactive protein levels, ameliorated the times to the resolution of fever, cough, and lung rales, and increased the oxygenation index. The evidence indicated that TRQI combined with antibiotics caused no adverse reactions.

Conclusions: Our study showed that the combination of TRQI and antibiotics was effective for treating pulmonary infection after ICH. However, high-quality multicenter RCTs are needed to further verify the clinical efficacy of TRQI due to the publication bias and the low methodological quality of the included RCTs.
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http://dx.doi.org/10.1097/MD.0000000000024905DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7982207PMC
March 2021

Xuesaitong exerts long-term neuroprotection for stroke recovery by inhibiting the ROCKII pathway, in vitro and in vivo.

J Ethnopharmacol 2021 May 20;272:113943. Epub 2021 Feb 20.

Key Laboratory of Chinese Internal Medicine of Educational Ministry and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, 100700, Beijing, China; Department of Neurology, Dongzhimen Hospital, Beijing University of Chinese Medicine, 100700, Beijing, China. Electronic address:

Ethnopharmacological Relevance: Xuesaitong (XST) is a traditional Chinese medicine injection with neuroprotective properties and has been extensively used to treat stroke for many years. The main component of XST is Panax notoginseng saponins (PNS), which is the main extract of the Chinese herbal medicine Panax notoginseng.

Aim Of The Study: In this study, we investigated whether XST provided long-term neuroprotection by inhibiting neurite outgrowth inhibitor-A (Nogo-A) and the ROCKII pathway in experimental rats after middle cerebral artery occlusion (MCAO) and in SH-SY5Y cells exposed to oxygen-glucose deprivation/reperfusion (OGD/R).

Materials And Methods: Rats with permanent MCAO were administered XST, Y27632, XST plus Y27632, and nimodipine for 14 and 28 days. Successful MCAO onset was confirmed by 2,3,5-triphenyl tetrazolium chloride (TTC) staining. Neurological deficit score (NDS) was used to assess neurological impairment. Hematoxylin-eosin (HE) staining and immunohistochemical (IHC) analysis of synaptophysin (SYN) and postsynaptic density protein-95 (PSD-95) were performed to evaluate cerebral ischemic injury and the neuroprotective capability of XST. Nogo-A levels and the ROCKII pathway were detected by IHC analysis, western blotting, and quantitative real-time polymerase chain reaction (qRT-PCR) to explore the protective mechanism of XST. OGD/R model was established in SH-SY5Y cells. Cell counting kit 8 (CCK8) was applied to detect the optimum OGD time and XST concentration. The expression levels Nogo-A and ROCKII pathway were determined using western blotting.

Results: Our results showed that XST reduced neurological dysfunction and pathological damage, promoted weight gain and synaptic regeneration, reduced Nogo-A mRNA and protein levels, and inhibited the ROCKII pathway in MCAO rats. CCK8 assay displayed that the optimal OGD time and optimal XST concentration were 7 h and 20 μg/mL respectively in SH-SY5Y cells. XST could evidently inhibit OGD/R-induced Nogo-A protein expression and ROCKII pathway activation in SH-SY5Y cells.

Conclusions: The present study suggested that XST exerted long-term neuroprotective effects that assisted in stroke recovery, possibly through inhibition of the ROCKII pathway.
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http://dx.doi.org/10.1016/j.jep.2021.113943DOI Listing
May 2021

Clinical Efficacy of Tonic Traditional Chinese Medicine Injection on Acute Cerebral Infarction: A Bayesian Network Meta-Analysis.

Evid Based Complement Alternat Med 2020 23;2020:8318792. Epub 2020 Nov 23.

Key Laboratory of Chinese Internal Medicine of Educational Ministry and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.

Western medicine (WM) has certain limitations in terms of treating acute cerebral infarction (ACI), while tonic traditional Chinese medicine injections (TCMIs) have been shown to have obvious clinical effects as an adjunct to WM for ACI. However, most randomized controlled trials (RCTs) to date have not performed direct comparisons of efficacy among tonic TCMIs. This study designed a Bayesian network meta-analysis (NMA) to explore the therapeutic effect of tonic TCMIs on ACI. A comprehensive search of RCTs of TCMIs combined with WM for ACI was conducted using electronic databases for studies dated from the start date of each database until February 2020. Stata 13.0 and ADDIS 1.16.7 software were used to plot and analyze the data. Sixty-six RCTs with a total of 5,989 patients involving 7 kinds of tonic TCMIs were included. Among TCMIs, Shenfu injection (SFI) + WM ranked first in terms of improving clinical efficacy and the activities of daily living (ADLs) rating and reducing interleukin-6 (IL-6) and tumor necrosis factor- (TNF-) levels. While Ciwujia injection (CI) + WM was the best choice for reducing neurological impairment and the high-cut viscosity of whole blood (HCV). Shenmai injection (SI) + WM had the greatest effects in terms of decreasing the levels of low-cut viscosity of whole blood (LCV), fibrinogen (FIB), and plasma viscosity (PV). Based on the cluster analysis of the clinical efficacy and the neurological impairment, CI + WM and Shenqifuzheng (SQI) + WM were the best options for treating ACI. With respect to adverse drug reactions (ADRs), 35 RCTs did not monitor ADRs during treatment. In conclusion, tonic TCMIs could assist WM in benefiting patients with ACI. However, due to the limitations of the current study, strict monitoring of ADRs and data from high-quality RCTs will be required in future to verify the advantage of TCMIs.
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http://dx.doi.org/10.1155/2020/8318792DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7704142PMC
November 2020

Revealing the Pharmacological Mechanism of in the Treatment of Ischemic Stroke Based on Network Pharmacology.

Evid Based Complement Alternat Med 2020 31;2020:3236768. Epub 2020 Oct 31.

Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China.

Aim: Stroke is the second significant cause for death, with ischemic stroke (IS) being the main type threatening human being's health. (AT) is widely used in the treatment of Alzheimer disease, epilepsy, depression, and stroke, which leads to disorders of consciousness disease. However, the systemic mechanism of AT treating IS is unexplicit. This article is supposed to explain why AT has an effect on the treatment of IS in a comprehensive and systematic way by network pharmacology.

Methods And Materials: ADME (absorbed, distributed, metabolized, and excreted) is an important property for screening-related compounds in AT, which were screening out of TCMSP, TCMID, Chemistry Database, and literature from CNKI. Then, these targets related to screened compounds were predicted via Swiss Targets, when AT-related targets database was established. The gene targets related to IS were collected from DisGeNET and GeneCards. IS-AT is a common protein interactive network established by STRING Database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were analysed by IS-AT common target genes. Cytoscape software was used to establish a visualized network for active compounds-core targets and core target proteins-proteins interactive network. Furthermore, we drew a signal pathway picture about its effect to reveal the basic mechanism of AT against IS systematically.

Results: There were 53 active compounds screened from AT, inferring the main therapeutic substances as follows: bisasaricin, 3-cyclohexene-1-methanol-,,4-trimethyl,acetate, ,,-7,10,13-hexadecatrienal, hydroxyacoronene, nerolidol, galgravin, veraguensin, 2'-o-methyl isoliquiritigenin, gamma-asarone, and alpha-asarone. We obtained 398 related targets, 63 of which were the same as the IS-related genes from targets prediction. Except for GRM2, remaining 62 target genes have an interactive relation, respectively. The top 10 degree core target genes were IL6, TNF, IL1B, TLR4, NOS3, MAPK1, PTGS2, VEGFA, JUN, and MMP9. There were more than 20 terms of biological process, 7 terms of cellular components, and 14 terms of molecular function through GO enrichment analysis and 13 terms of signal pathway from KEGG enrichment analysis based on < 0.05.

Conclusion: AT had a therapeutic effect for ischemic via multicomponent, multitarget, and multisignal pathway, which provided a novel research aspect for AT against IS.
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http://dx.doi.org/10.1155/2020/3236768DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7648688PMC
October 2020

In Vitro Evaluation of the Neuroprotective Effect of Saponins by Activating the EGFR/PI3K/AKT Pathway.

Evid Based Complement Alternat Med 2020 31;2020:1403572. Epub 2020 Jul 31.

Key Laboratory of Chinese Internal Medicine of Educational Ministry and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.

Objective: This study investigated whether saponins (PNS) extracted from (Bruk.) F. H. Chen played a neuroprotective role by affecting the EGFR/PI3K/AKT pathway in oxygen-glucose deprived (OGD) SH-SY5Y cells.

Materials And Methods: Different groups of OGD SH-SY5Y cells were treated with varying doses of PNS, PNS + AG1478 (a specific inhibitor of EGFR), or AG1478 for 16 hours. CCK8, Annexin V-FITC/PI apoptosis analysis, and LDH release analysis were used to determine cell viability, apoptosis rate, and amounts of LDH. Quantitative real-time PCR (q-RT-PCR) and western blotting were used to measure mRNA and proteins levels of p-EGFR/EGFR, p-PI3K/PI3K, and p-AKT/AKT in SH-SY5Y cells subjected to OGD.

Results: PNS significantly enhanced cell viability, reduced apoptosis, and weakened cytotoxicity by inhibiting the release of LDH. The mRNA expression profiles of EGFR, PI3K, and AKT showed no difference between model and other groups. Additionally, ratios of p-EGFR, p-PI3K, and p-AKT to EGFR, PI3K, and AKT proteins expression, respectively, all increased significantly.

Conclusions: These findings indicate that PNS enhanced neuroprotective effects by activating the EGFR/PI3K/AKT pathway and elevating phosphorylation levels in OGD SH-SY5Y cells.
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http://dx.doi.org/10.1155/2020/1403572DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7415117PMC
July 2020

NOS1 expression promotes proliferation and invasion and enhances chemoresistance in ovarian cancer.

Oncol Lett 2020 Apr 27;19(4):2989-2995. Epub 2020 Jan 27.

Cancer Research Institute, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.

Nitric oxide (NO), an important chemical messenger, serves a dual role in tumor progression. Nitric oxide synthase isoform 1 (NOS1) was observed to be increasingly expressed in various types of cancer, and its expression has been associated with tumor progression. However, the level of NOS1 expression and the associated functions of NOS1 in human ovarian cancer remain undefined. Using gene expression profiles of ovarian cancer from the Gene Expression Omnibus (GEO) database, the present study revealed that NOS1 was increasingly expressed in ovarian cancer tissues. The present study investigated the level of NOS1 expression and its effects on cell function, including proliferation, migration and invasion as well as chemoresistance to cispatin (DDP) treatment in OVCAR3 cells. Reverse transcription-quantitative polymerase chain reaction demonstrated that the level of NOS1 mRNA expression varied in different ovarian cancer lines. However, immunoblotting indicated that the level of NOS1 protein expression was constitutively high in ovarian cancer cell lines. Treatment with NOS inhibitor NG-nitro-L-arginine methyl ester or transfection with NOS1 short hairpin RNA significantly inhibited cell proliferation, migration and invasion compared with the control, whereas the sensitivity of OVCAR3 cells to DDP treatment was increased. The results of the present study indicated that NOS1 promoted the function of ovarian cancer cells, including proliferation, invasion and chemoresistance, providing a potential target for ovarian cancer therapeutic.
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http://dx.doi.org/10.3892/ol.2020.11355DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7068236PMC
April 2020

PTEN S-nitrosylation by NOS1 inhibits autophagy in NPC cells.

Cell Death Dis 2019 04 5;10(4):306. Epub 2019 Apr 5.

Cancer Research Institute, Southern Medical University, 1838 Guangzhou road north, Guangzhou, Guangdong, China.

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http://dx.doi.org/10.1038/s41419-019-1542-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6451008PMC
April 2019

Publisher Correction: NOS1 S-nitrosylates PTEN and inhibits autophagy in nasopharyngeal carcinoma cells.

Cell Death Dis 2019 Mar 25;10(4):286. Epub 2019 Mar 25.

Cancer Research Institute, Southern Medical University, Guangzhou, China.

It was brought to the attention of the Editors that there had been an accidental duplication of the western blot images during the preparation of Figs. 1b and c. The authors were notified about the error and have supplied the correct image for Fig. 1c (below). We apologize for any inconvenience this may have caused readers.
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http://dx.doi.org/10.1038/s41419-019-1476-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6433868PMC
March 2019

Piperidine nitroxide Tempol enhances cisplatin-induced apoptosis in ovarian cancer cells.

Oncol Lett 2018 Oct 10;16(4):4847-4854. Epub 2018 Aug 10.

Cancer Research Institute, School of Basic Medical Science, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.

A nitroxide radical, Tempol (Tempol, TPL), is usually used as an antioxidative agent clinically, whereas the mechanism underlying its pro-oxidative effect has not been thoroughly investigated. The present study investigated the pro-oxidative effect of TPL on the inhibition of cellular proliferation and its role in enhancing the effect of anticancer drug cisplatin (DDP) on the induction of apoptosis in ovarian cancer cells. Cell viability and proliferation were evaluated by MTT assay. Cell apoptosis was analyzed by flow cytometry (FCM) following staining with Annexin V/propidium iodide. Western blot analysis was performed to determine the expression levels of anti-apoptotic protein B-cell lymphoma-2 (Bcl-2) and pro-apoptotic protein Bcl-2-associated X protein (Bax), and the Bcl-2:Bax expression ratio. Cellular reactive oxygen species (ROS) were labeled with dichlorofluorescin-diacetate and analyzed by FCM. The results revealed that cell viabilities of OVCAR3 and SKOV3 cells were decreased by TPL in dose-dependent manner at concentrations of 2 to 10 mM after 48 h incubation. The cell proliferation rates of OVCAR3 and SKOV3 cells were suppressed by TPL at lower toxic concentrations of 1.5 and 1 mM, respectively, compared with the control group. The MTT assay indicated that the combination therapy significantly inhibited the cell proliferation of OVCAR3 cells compared with treatment with DDP alone. FCM demonstrated that the combination treatment increased the proportion of early apoptotic cells in OVCAR3 cells compared with single DDP treatment. Western blot analysis revealed that the combination treatment markedly decreased the Bcl-2:Bax expression ratio compared with treatment with DDP alone. Detection of cellular ROS expression levels demonstrated that the combination therapy significantly increased cellular ROS generation compared with the DDP-only therapy. These data indicated that TPL increased the effect of DDP on inducing apoptosis in OVCAR3 cells.
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http://dx.doi.org/10.3892/ol.2018.9289DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6144655PMC
October 2018

The Mechanism of Exosomes Function in Neurological Diseases: A Progressive Review.

Curr Pharm Des 2018 ;24(24):2855-2861

Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.

Exosomes are extracellular microparticles (≈30-100 nm in diameter) secreted from nearly all types of cells, containing a whole set of biological information including proteins, ribonucleic acid (RNA) and lipids. Latest studies show that exosomes contribute to cell-cell communication and are considered closely related with the modulation of angiogenesis and neurogenesis in many neurological diseases. In the past decade, numerous researchers were devoted to exosomes study, but the mechanism of exosomes function and delivery is uncertain. In this review, we summarized several potential mechanisms of exosomes function in angiogenesis, neurogenesis and Blood Brain Barrier (BBB) delivery, and differentiate various sources of exosomes in stroke, tumor, Traumatic Brain Injury (TBI) and Alzheimer's Disease (AD) aimed to report the most advanced mechanical theories in related past three years to provide a new sight for this research area.
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http://dx.doi.org/10.2174/1381612824666180903113136DOI Listing
October 2019

Chinese Herbal Formula, Modified Danggui Buxue Tang, Attenuates Apoptosis of Hematopoietic Stem Cells in Immune-Mediated Aplastic Anemia Mouse Model.

J Immunol Res 2017 16;2017:9786972. Epub 2017 Aug 16.

Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China.

A derivative formula, DGBX, which is composed of three herbs (, , and Franch), is derived from a famous Chinese herbal formula, Danggui Buxue Tang (DBT) ( and ). We aimed to investigate the effects of DGBX on the regulation of the balance between proliferation and apoptosis of hematopoietic stem cells (HSCs) due to the aberrant immune response in a mouse model of aplastic anemia (AA). Cyclosporine (CsA), an immunosuppressor, was used as the positive control. Our results indicated that DGBX could downregulate the production of IFN in bone marrow cells by interfering with the binding between SLAM and SAP and the expressions of Fyn and T-bet. This herbal formula can also inhibit the activation of Fas-mediated apoptosis, interferon regulatory factor-1-induced JAK/Stat, and eukaryotic initiation factor 2 signaling pathways and thereby induce proliferation and attenuate apoptosis of HSCs. In conclusion, DGBX can relieve the immune-mediated destruction of HSCs, repair hematopoietic failure, and recover the hematopoietic function of HSCs in hematogenesis. Therefore, DGBX can be used in traditional medicine against AA as a complementary and alternative immunosuppressive therapeutic formula.
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http://dx.doi.org/10.1155/2017/9786972DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5603747PMC
July 2018

The herbal decoction modified Danggui Buxue Tang attenuates immune-mediated bone marrow failure by regulating the differentiation of T lymphocytes in an immune-induced aplastic anemia mouse model.

PLoS One 2017 6;12(7):e0180417. Epub 2017 Jul 6.

Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.

Angelicae Sinensis, Radix Astragali and Rhizoma Coptidis are all herbs of modified Danggui Buxue Tang (DGBX) and are extensively applied herbs in traditional Chinese medicine for the treatment of anemia and inflammation. In this study, immune-induced AA mice were used as an animal model, and the immunosuppressive agent, Ciclosporin A (CsA), was used as a positive control. Multiple pro-inflammatory cytokines were examined by bead-based multiplex flow cytometry. The T-cell subsets were assessed using a fluorescence-activated cell sorter (FACS). Western blot analysis was used to estimate the protein expression levels of specific transcription factors for T helper cells (Th1, Th2 and Th17) and key molecules of the Janus-activated kinase (Jak)/signal transducer and activator of transcription (Stat3) signaling pathway. DGBX treatment could significantly increase the production of whole blood cells in peripheral blood (PB); inhibit the expansion of Th1 and Th17 cells; increase the differentiation of Th2 and Tregs cells; regulate the expression levels of T-bet, GATA-3, RORγ and proinflammatory cytokines; and decrease the expression levels of key molecules in the Jak/Stat signaling pathway. These results indicate that DGBX can regulate the differentiation of T lymphocytes, resulting in immunosuppressive and hematogenic functions on AA mice. DGBX might be a good candidate for inclusion in a randomized study for AA with more data on the possible side effects and doses used in humans. Ultimately, it may be used for applications of traditional medicine against AA in modern complementary and alternative immunosuppressive therapeutics.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0180417PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5500321PMC
September 2017

A Systematic Review and Meta-Analysis on the Treatment of Cerebral Hemorrhage with NaoXueShu Oral Liquid.

Biomed Res Int 2017 29;2017:8542576. Epub 2017 May 29.

Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Key Office of Encephalopathy TCM Research, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.

NaoXueShu oral liquid invigorates Qi and promotes blood circulation, which is mainly used for treating the acute stage of the meridian of hemorrhagic apoplexy and acute blood stasis syndrome during early convalescence. Its main clinical manifestations include hemiplegia, mouth askew, hemianesthesia, and inarticulateness. It is used mainly in patients with lobar hemorrhage, basal ganglia, and thalamus of the small amount of bleeding without disturbing consciousness of hypertensive cerebral. The purpose of this study was to evaluate the efficacy and adverse effects of NaoXueShu oral liquid on the treatment of cerebral hemorrhage. In this study, literature on randomized controlled trials was collected from seven databases to evaluate the clinical efficiency of the treatment of cerebral hemorrhage alone or combined with Western medicine. The methodologic quality of the included studies was assessed using a standard Cochrane system review and analyzed using RevMan 5.3.0 software. The study included 14 eligible randomized controlled trials. The results showed that the use of NaoXueShu oral liquid alone or combined with other drugs or auxiliary methods can play a significant role in the treatment of cerebral hemorrhage, especially hypertensive intracerebral hemorrhage.
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http://dx.doi.org/10.1155/2017/8542576DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5467282PMC
March 2018

iNOS-derived nitric oxide promotes glycolysis by inducing pyruvate kinase M2 nuclear translocation in ovarian cancer.

Oncotarget 2017 May;8(20):33047-33063

Cancer Research Institute, Southern Medical University, Guangzhou 510515, China.

Aerobic glycolysis is essential for tumor growth and survival. Activation of multiple carcinogenic signals contributes to metabolism reprogramming during malignant transformation of cancer. Recently nitric oxide has been noted to promote glycolysis but the mechanism remains elusive. We report here the dual role of nitric oxide in glycolysis: low/physiological nitric oxide (≤ 100 nM) promotes glycolysis for ATP production, oxidative defense and cell proliferation of ovary cancer cells, whereas excess nitric oxide (≥ 500 nM) inhibits it. Nitric oxide has a positive effect on glycolysis by inducing PKM2 nuclear translocation in an EGFR/ERK2 signaling-dependent manner. Moreover, iNOS induced by mild inflammatory stimulation increased glycolysis and cell proliferation by producing low doses of nitric oxide, while hyper inflammation induced iNOS inhibited it by producing excess nitric oxide. Finally, iNOS expression is abnormally increased in ovarian cancer tissues and is correlated with PKM2 expression. Overexpression of iNOS is associated with aggressive phenotype and poor survival outcome in ovarian cancer patients. Our study indicated that iNOS/NO play a dual role of in tumor glycolysis and progression, and established a bridge between iNOS/NO signaling pathway and EGFR/ERK2/PKM2 signaling pathway, suggesting that interfering glycolysis by targeting the iNOS/NO/PKM2 axis may be a valuable new therapeutic approach of treating ovarian cancer.
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http://dx.doi.org/10.18632/oncotarget.16523DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5464849PMC
May 2017

NOS1 -nitrosylates PTEN and inhibits autophagy in nasopharyngeal carcinoma cells.

Cell Death Discov 2017 20;3:17011. Epub 2017 Feb 20.

Cancer Research Institute, Southern Medical University , Guangzhou, China.

Autophagy is a cellular survival mechanism that involves the catabolic degradation of damaged proteins and organelles during periods of metabolic stress, and when overly stimulated, commonly contributes to cell death. Nitric oxide (NO), a potent cellular messenger, participates in a complex mechanism which assists in controlling autophagy. However, the mechanism by which endogenous NO formed by distinct isoforms of nitric oxide synthase (NOS) helps to regulate autophagy in cancer cells remains unclear. Here we report that NOS1 reduces excessive levels of autophagy and promotes the survival of nasopharyngeal carcinoma cells. We found that inhibition of NOS1 increased cell death resulting from siRNA or the use of pharmacologic agents; and this effect was reversed by the autophagy inhibitor, chloroquine. The role of NOS1 in the autophagy process depended on the activation of AKT/mTOR signaling by -nitrosylation of phosphatase and tensin homolog (PTEN) proteins. The mechanism by which NOS1 modifies PTEN protein might involve a direct interaction between these two molecules. Moreover, in an study, the NOS1 inhibitor N(G)-nitro-L-arginine methyl ester activated AKT/mTOR signaling and promoted autophagy in xenograph tumors. Our studies demonstrated that NOS1 prevents excessive autophagy via -nitrosylation of PTEN, and activation of the AKT/mTOR signaling pathway. PTEN and the AKT/mTOR signaling pathway are promising targets for improving the chemotherapeutic treatment of cancer.
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http://dx.doi.org/10.1038/cddiscovery.2017.11DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5317009PMC
February 2017

Herbal formula Xian-Fang-Huo-Ming-Yin regulates differentiation of lymphocytes and production of pro-inflammatory cytokines in collagen-induced arthritis mice.

BMC Complement Altern Med 2017 Jan 5;17(1):12. Epub 2017 Jan 5.

Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Haiyuncang Hutong No.5, , Dongcheng District, Beijing, China.

Background: Xian-Fang-Huo-Ming-Yin (XFHM), a traditional herbal formula, has been used to treat sores and carbuncles for hundreds of years in Asia. Nowadays, its clinical effects in treatment of rheumatoid arthritis (RA) have been validated. In this study, we want to study its possible molecular mechanisms of regulating the differentiation of lymphocytes and production of pro-inflammatory cytokines in collagen-induced arthritis (CIA) mice for RA treatment.

Methods: A high performance liquid chromatography-electrospray ionization/mass spectrometer (HPLC-ESI/MS) system was used to analyze the constituents of XFHM granules. An arthritics mouse model was induced by collagen and leflunomide (LEF) was used as a positive control medicine. Pathological changes at the metatarsophalangeal joint were studied through Safranin O and immunohistochemical staining. The differentiation of T, B and NK cells was examined by flow cytometry and pro-inflammatory cytokines were assayed using an Inflammation Antibody Array assay. The expression of key molecules of the nuclear factor κB (NF-κB) and Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathways in spleen were studied by western-blot analysis.

Results: In our study. 21 different dominant chemical constituents were identified in XFHM. Treatment with XFHM suppressed the pathological changes in arthrosis of CIA. Additionally, XFHM down-regulated the proliferation and differentiation of CD3 T cells and CD3CD19 B cells significantly. However, XFHM had no significant effect on CD3NK1.1 NK cells. Further study showed that the production of pro-inflammatory cytokines had been suppressed by inhibiting the activation of NF-κB and JAK/STAT signaling.

Conclusions: XFHM can regulate and maintain the immunologic balance of lymphocytic immunity and inhibit the production of pro-inflammatory cytokines, thus suppressing the pathological changes of RA. Therefore, XFHM may be used as an application of traditional medicine against RA in modern complementary and alternative therapeutics.
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http://dx.doi.org/10.1186/s12906-016-1526-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5216578PMC
January 2017

Xianfanghuomingyin, a Chinese Compound Medicine, Modulates the Proliferation and Differentiation of T Lymphocyte in a Collagen-Induced Arthritis Mouse Model.

Evid Based Complement Alternat Med 2016 30;2016:6356871. Epub 2016 Aug 30.

Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.

In traditional Chinese medicine (TCM), xianfanghuomingyin (XFHM) is used to treat autoimmune diseases, including rheumatoid arthritis (RA). Here, we studied the mechanisms underlying its treatment effects, especially its anti-inflammatory effects in a collagen-induced arthritis (CIA) mouse model. We found that cartilage destruction and pannus formation were alleviated by treatment with XFHM. The abnormal differentiation of Th1 and Th17 cells was downregulated significantly by XFHM, and Th2 and Treg cells were upregulated. Moreover, the expression levels of specific cytokines and transcription factors related to Th1 cells (interferon γ [IFNγ], T-bet) and Th17 cells (interleukin- [IL-] 17) and the nuclear receptor retinoic acid receptor-related orphan receptor-gamma (RORγ) were downregulated. Serum IL-4 and GATA-3, which contribute to Th2 cells differentiation, increased significantly after XFHM administration. These results indicate that XFHM can restore the balance of T lymphocytes and reestablish the immunological tolerance to inhibit autoinflammatory disorder of RA. Taken together, XFHM can be used as a complementary or alternative traditional medicine to treat RA.
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http://dx.doi.org/10.1155/2016/6356871DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5021507PMC
September 2016

Panax notoginseng saponins administration modulates pro- /anti-inflammatory factor expression and improves neurologic outcome following permanent MCAO in rats.

Metab Brain Dis 2017 02 2;32(1):221-233. Epub 2016 Sep 2.

Key Laboratory of Chinese Internal Medicine of Educational Ministry and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.

Ischemic stroke, particularly permanent occlusion, accounts for the overwhelming majority of all strokes. In addition to the occlusion of arteries, the inflammatory response plays a pivotal role in the severity of the cerebral injury and its clinical prognosis. Here, panax notoginseng saponins (PNS) extracted from a traditional Chinese herbal medicine was administered following permanent middle cerebral artery occlusion (MCAO) in rats to explore the neuroprotective mechanisms against ischemic injury. The results showed that MCAO surgery was successful in producing an infarct and that PNS and nimodipine could ameliorate the neurological deficits. The expression levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and transforming growth factor-β1 (TGF-β1) were increased, while the level of interleukin-10 (IL-10) was reduced in the infarct cortex 7 days after MCAO, as assessed by immunohistochemistry, western blotting and quantitative real-time PCR (qRT-PCR). PNS was able to markedly reduce the overexpression of IL-1β and TNF-α while significantly promoting the expression of IL-10, but did not affect the elevated expression of TGF-β1. Meanwhile, nimodipine was able to significantly reduce the expression of IL-1β and TNF-α, but had no obvious effect on IL-10 or TGF-β1. In addition, the serum levels of TNF-α, IL-10 and TGF-β1 were basically consistent with cerebral tissue results; however, the IL-1β levels did not differ. We conclude that PNS can directly down-regulate the overexpression of proinflammatory factors IL-1β and TNF-α while up-regulating the expression of anti-inflammatory factor IL-10 in the core region of the cerebral infarct, thereby preventing neurological damage in rats after permanent MCAO.
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http://dx.doi.org/10.1007/s11011-016-9901-3DOI Listing
February 2017

Panax notoginseng saponins provide neuroprotection by regulating NgR1/RhoA/ROCK2 pathway expression, in vitro and in vivo.

J Ethnopharmacol 2016 Aug 8;190:301-12. Epub 2016 Jun 8.

Key Laboratory of Chinese Internal Medicine of Educational Ministry and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China. Electronic address:

Ethnopharmacological Relevance: Panax notoginseng saponins (PNS) extracted from a traditional Chinese herbal medicine, Panax notoginseng (Burkill) F.H. Chen (Araliaceae), which has been extensively used in treating coronary heart disease, ischemic cerebrovascular disease and hemorrhagic disorders in China over hundreds of years.

Aims Of The Study: This study explored whether panax notoginseng saponins (PNS) provided neuroprotective effects by inhibiting the expressions of NgR1, RhoA, and ROCK2 following middle cerebral artery occlusion in rats and oxygen-glucose deprivation/reoxygenation (OGD/R) injury in SH-SY5Y cells.

Materials And Methods: 2,3,5-Triphenyltetrazolium chloride staining was used to determine successful middle cerebral artery occlusion establishment in sham-operated and operated Sprague-Dawley rats 1 day after injury. The rats were randomly separated into sham, model, NEP1-40, PNS, and NEP1-40 plus PNS (N+P) groups. After 7 days of treatment, body mass and neurological deficit scores were analyzed. Tissues were harvested and analyzed by hematoxylin-eosin staining and immunohistochemical analysis, western blotting, and quantitative real-time PCR (qRT-PCR). The optimal drug concentration of NEP1-40 and PNS on SH-SY5Y cells exposed to OGD/R injury was determined by CCK8 analysis. qRT-PCR was used to measure mRNA expression profiles of NgR1, RhoA, and ROCK2 in SH-SY5Y cells subjected to OGD/R.

Results: The results showed that MCAO surgery successfully produced an infarct, and the PNS, NEP1-40, and N+P groups exhibited increased body mass and ameliorated neurological deficits compared with the model group. NEP1-40 treatment markedly reduced NgR1 and RhoA overexpression when compared to the model group, although there was no significant difference in ROCK2 expression. PNS and N+P treatment significantly decreased NgR1, RhoA, and ROCK2 overexpression compared with the model group. However, N+P treatment did not result in a synergistic effect, as assessed by immunohistochemistry, western blotting, and qRT-PCR. Following optimal administration of PNS (160μg/ml) and NEP1-40 (10ng/ml) on SH-SY5Y cells exposed to OGD/R injury, cell viability in the NEP1-40, PNS, and N+P groups significantly increased compared with the model group, as assessed by CCK8 analysis. Additionally, NgR1, RhoA, and ROCK2 mRNA expression profiles were significantly less in the NEP1-40, PNS, and N+P groups compared with the model group.

Conclusion: PNS provided neuroprotective effects in a rat model of cerebral ischemia and SH-SY5Y cells exposed to oxygen/glucose deprivation injury by inhibiting the overexpression of NgR1, RhoA, and ROCK2.
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http://dx.doi.org/10.1016/j.jep.2016.06.017DOI Listing
August 2016

Chlorogenic acid induces apoptosis to inhibit inflammatory proliferation of IL-6-induced fibroblast-like synoviocytes through modulating the activation of JAK/STAT and NF-κB signaling pathways.

Exp Ther Med 2016 May 9;11(5):2054-2060. Epub 2016 Mar 9.

Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, P.R. China.

Chlorogenic acid (CGA) is the primary constituent of Caulis , a Chinese herb used for the treatment of rheumatoid arthritis (RA). The present study aimed to investigate whether CGA was able to inhibit the proliferation of the fibroblast-like synoviocyte cell line (RSC-364), stimulated by interleukin (IL)-6, through inducing apoptosis. Following incubation with IL-6 or IL-6 and CGA, the cellular proliferation of RSC-364 cells was detected by MTT assay. The ratio of apoptosed cells were detected by flow cytometry. Western blot analysis was performed to observe protein expression levels of key molecules involved in the Janus-activated kinase/signal transducer and activator of transcription 3 (JAK/STAT) signaling pathway [phosphorylated (p)-STAT3, JAK1 and gp130] and the nuclear factor κB (NF-κB) signaling pathway [phosphorylated (p)-inhibitor of κB kinase subunit α/β and NF-κB p50). It was revealed that CGA was able to inhibit the inflammatory proliferation of RSC-364 cells mediated by IL-6 through inducing apoptosis. CGA was also able to suppress the expression levels of key molecules in the JAK/STAT and NF-κB signaling pathways, and inhibit the activation of these signaling pathways in the inflammatory response through IL-6-mediated signaling, thereby resulting in the inhibition of the inflammatory proliferation of synoviocytes. The present results indicated that CGA may have potential as a novel therapeutic agent for inhibiting inflammatory hyperplasia of the synovium through inducing synoviocyte apoptosis in patients with RA.
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http://dx.doi.org/10.3892/etm.2016.3136DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4840502PMC
May 2016

Meta-Analysis of the Effects of Xingnaojing Injection on Consciousness Disturbance.

Medicine (Baltimore) 2016 Feb;95(7):e2875

From the Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing (LW, YG, XR, BN, LZ, HS); Key office of Encephalopathy TCM Research (LW, HZ, YG, LZ, Ying Gao), State Administration of Traditional Chinese Medicine, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine; Guang'anmen Hospital (YX, YL), Chinese Academy of Chinese Medical Sciences, Beijing; and Shandong University of Traditional Chinese Medicine (JL), Jinan, China.

Xingnaojing (XNJ) is commonly extracted from Angongniuhuang, a classic Chinese emergency prescription, and widely used in the treatment of nervous system disorders including consciousness disturbance in China. To evaluate the beneficial and adverse effects of XNJ injection, on consciousness disturbance. Seven major electronic databases were searched to retrieve randomized controlled trials designed to evaluate the clinical efficacy of XNJ alone or combined with Western medicine in treating consciousness disturbance caused by conditions such as high fever, poisoning, and stroke. The methodological quality of the included studies was assessed using criteria from the Cochrane Handbook for Systematic Review of Interventions, and analyzed using the RevMan 5.3.0 software. Seventeen randomized controlled trials on XNJ were included in this study and the trials generally showed low methodological quality. The results revealed that XNJ alone or in combination with other medicines and adjuvant methods had a positive effect on patients with fever-, poisoning-, and stroke-induced coma. XNJ effectively treated consciousness disturbances that were caused by high fever, poisoning, or stroke.
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http://dx.doi.org/10.1097/MD.0000000000002875DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4998655PMC
February 2016

Identification of key genes in hepatocellular carcinoma and validation of the candidate gene, cdc25a, using gene set enrichment analysis, meta-analysis and cross-species comparison.

Mol Med Rep 2016 Feb 7;13(2):1172-8. Epub 2015 Dec 7.

Department of Research, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.

The aim of the present study was to determine key pathways and genes involved in the pathogenesis of hepatocellular carcinoma (HCC) through bioinformatic analyses of HCC microarray data based on cross-species comparison. Microarray data of gene expression in HCC in different species were analyzed using gene set enrichment analysis (GSEA) and meta-analysis. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to determine the mRNA and protein expression levels of cdc25a, one of the identified candidate genes, in human, rat and tree shrew samples. The cell cycle pathway had the largest overlap between the GSEA and meta-analysis. Meta-analyses showed that 25 genes, including cdc25a, in the cell cycle pathway were differentially expressed. Cdc25a mRNA levels in HCC tissues were higher than those in normal liver tissues in humans, rats and tree shrews, and the expression level of cdc25a in HCC tissues was higher than in corresponding paraneoplastic tissues in humans and rats. In human HCC tissues, the cdc25a mRNA level was significantly correlated with clinical stage, portal vein tumor thrombosis and extrahepatic metastasis. Western blotting showed that, cdc25a protein levels were significantly upregulated in HCC tissues in humans, rats and tree shrews. In conclusion, GSEA and meta-analysis can be combined to identify key molecules and pathways involved in HCC. This study demonstrated that the cell cycle pathway and the cdc25a gene may be crucial in the pathogenesis and progression of HCC.
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http://dx.doi.org/10.3892/mmr.2015.4646DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4732839PMC
February 2016

Panax notoginseng saponins promotes stroke recovery by influencing expression of Nogo-A, NgR and p75NGF, in vitro and in vivo.

Biol Pharm Bull 2014 ;37(4):560-8

The spontaneous recovery of function after injury in the adult central nervous system is limited due to the several proteins, such as Nogo-A that have repulsive or inhibitory effects on growing neuritis. The Chinese herbal medicine extraction Panax notoginseng saponins (PNS) injection has been widely used and effective in repairing the function of impaired nerves, but the mechanism of this herbal medicine is still poorly understood. This project evaluated the effect of Panax notoginseng saponins on neurological functional recovery and on the expression of Nogo-A, NgR and p75 at 7, 14 and 28 d after middle cerebral artery occlusion (MCAO) in rats and also oxygen-glucose deprivation/reperfusion (OGD/R) model on SH-SY5Y cells. We found that the expression of Nogo-A, NgR and p75 of rats receiving MCAO surgery increased on the 7th day, reached a peak on the 14th or 28th day and maintained high levels and Panax notoginseng saponins significantly decreased these expressions. This may be the mechanism of Panax notoginseng saponins that contributes to the recovery of nerve function, which plays an important role in brain protection after cerebral infarction.
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http://dx.doi.org/10.1248/bpb.b13-00770DOI Listing
June 2015

Effect of wenxin granule on ventricular remodeling and myocardial apoptosis in rats with myocardial infarction.

Evid Based Complement Alternat Med 2013 13;2013:967986. Epub 2013 Aug 13.

Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.

Aim. To determine the effect of a Chinese herbal compound named Wenxin Granule on ventricular remodeling and myocardial apoptosis in rats with myocardial infarction (MI). Methods. Male Sprague-Dawley (SD) rats were randomly divided into four groups: the control group, the model group, the metoprolol group, and the Wenxin Granule group (WXKL group) with sample size (n) of 7 rats in each group. An MI model was established in all rats by occlusion of the left anterior descending coronary artery (the control group was without occlusion). Wenxin Granule (1.35 g/kg/day), metoprolol (12 mg/kg/day), and distilled water (5 mL/kg/day for the control and model groups) were administered orally for 4 weeks. Ultrasonic echocardiography was used to examine cardiac structural and functional parameters. Myocardial histopathological changes were observed using haematoxylin and eosin (H&E) dyeing. Myocardial apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) staining. Serum angiotensin II (Ang II) concentration was measured using the enzyme-linked immunosorbent assay (ELISA). Results. It was found that Wenxin Granule could partially reverse ventricular remodeling, improve heart function, alleviate the histopathological damage, inhibit myocardial apoptosis, and reduce Ang II concentration in rats with MI. Conclusions. The results of the current study suggest that Wenxin Granule may be a potential alternative and complementary medicine for the treatment of MI.
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http://dx.doi.org/10.1155/2013/967986DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3755410PMC
September 2013

The Correlation between High-Sensitivity C-Reactive Protein, Matrix Metallopeptidase 9, and Traditional Chinese Medicine Syndrome in Patients with Hypertension.

Evid Based Complement Alternat Med 2013 28;2013:780937. Epub 2013 Mar 28.

Key Laboratory of Chinese Internal Medicine of Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.

Hypertension is a common disease affecting millions of people throughout the world. Currently, there is a growing interest in the traditional Chinese medicine (TCM) for patients with hypertension mainly due to the personalized therapy of TCM in many countries. Clinical treatment of patients relies on the successful differentiation of a specific TCM syndrome for hypertension. However, it is difficult to understand that TCM syndrome classifications depend on the clinical experience of a TCM practitioner. Therefore, discovering an objective biomarker associated with TCM syndrome may be beneficial for TCM syndrome classifications. This paper focused on high sensitivity C-reactive protein (HCRP), matrix metallopeptidase 9 (MMP9), and TCM syndrome, and aimed to investigate the relationships between TCM syndrome and the two inflammatory biomarkers in patients with essential hypertension. The result showed that both HCRP and MMP9 are positively correlated with syndrome of wind and phlegm turbidity. Detection of the serum levels of HCRP and MMP9 is beneficial for TCM syndrome classification and prediction of cardiovascular and cerebrovascular risk events in hypertensive patients.
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http://dx.doi.org/10.1155/2013/780937DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625612PMC
April 2013

[Effect of Astragali Radix injection on myocardial cell mitochondrial structure and function in process of reversing myocardial cell hypertrophy].

Zhongguo Zhong Yao Za Zhi 2012 Apr;37(7):979-84

Key Laboratory of Chinese Internal Medicine of Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Traditional Chinese Medicine, Beijing 100700, China.

Objective: To study pathological and therapeutical problems concerning myocardial cell mitochondria changes during myocardial cell hypertrophy by culturing rat primary myocardial cells.

Method: Primary myocardial cells were seperated and cultured together with angiotensin II (Ang II) for 72 or 96 hours. The total protein content with the BCA method and the photography and measurement of cell diameter with inverted microscope reflected myocardial cell proliferation. The mitochondrial membrane potential (Delta Psi m) with fluorescence microscope, the mitochondrial single amine oxidase (MAO) activity with spectrophotometer, the mitochondrial cytochrome oxidase (COX) activity and the injury percentage of mitochondrial outer membrane with microplate reader and the contents of ATP, ADP, AMP with high performance liquid chromatography reflected the injury and energy metabolism of myocardial cell mitochondrial structure and function when being cultured together with Ang II. On that basis, cells were treated with Astragali Radix injection and valsartan for observing pharmacological effects on mitochondrial structure and function in restructured myocardial cells.

Result: In 72 h and 96 h, compare with the control group, the model group showed significantly increased total protein content and enlarged myocardial cell diameter. During the course of proliferation, the myocardial cell MAO activity and the injury percentage of mitochondrial outer membrane were significantly increased, with significant decrease in mitochondrial COX activity, mitochondrial Delta Psi m and the content of ATP, ADP and rise in the content of AMP. Astragali Radix injection and valsartan reduced myocardial cell total protein content and cell diameter caused by Ang II, decreased myocardial cell MAO activity, significantly increased mitochondrial COX activity and the content of ATP and ADP, and decreased the content of AMP.

Conclusion: During the process of myocardial hypertrophy, the injury of mitochondrial structure and function and the changes in myocardial cell energy metabolism injury occurred after the injury of mitochondria. Astragali Radix injection and valsartan can reverse myocardial cell mitochondrial structure and function during myocardial cell hypertrophy caused by Ang II. Reversion of myocardial cell hypertrophy and restructuring of myocardial cells helps improve energy metabolism of the myocardial cells.
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April 2012
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