Publications by authors named "Guang-Hui Wang"

75 Publications

Microglial MT1 activation inhibits LPS-induced neuroinflammation via regulation of metabolic reprogramming.

Aging Cell 2021 Jun 8;20(6):e13375. Epub 2021 May 8.

Department of Neurology, Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou, China.

Parkinson's disease (PD) is one of the most common neurodegenerative diseases. Although its pathogenesis remains unclear, a number of studies indicate that microglia-mediated neuroinflammation makes a great contribution to the pathogenesis of PD. Melatonin receptor 1 (MT1) is widely expressed in glia cells and neurons in substantia nigra (SN). Neuronal MT1 is a neuroprotective factor, but it remains largely unknown whether dysfunction of microglial MT1 is involved in the PD pathogenesis. Here, we found that MT1 was reduced in microglia of SN in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model. Microglial MT1 activation dramatically inhibited lipopolysaccharide (LPS)-induced neuroinflammation, whereas loss of microglial MT1 aggravated it. Metabolic reprogramming of microglia was found to contribute to the anti-inflammatory effects of MT1 activation. LPS-induced excessive aerobic glycolysis and impaired oxidative phosphorylation (OXPHOS) could be reversed by microglial MT1 activation. MT1 positively regulated pyruvate dehydrogenase alpha 1 (PDHA1) expression to enhance OXPHOS and suppress aerobic glycolysis. Furthermore, in LPS-treated microglia, MT1 activation decreased the toxicity of conditioned media to the dopaminergic (DA) cell line MES23.5. Most importantly, the anti-inflammatory effects of MT1 activation were observed in LPS-stimulated mouse model. In general, our study demonstrates that MT1 activation inhibits LPS-induced microglial activation through regulating its metabolic reprogramming, which provides a mechanistic insight for microglial MT1 in anti-inflammation.
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http://dx.doi.org/10.1111/acel.13375DOI Listing
June 2021

Lignans and phenylpropanoids from the roots of and their cytotoxic activities.

Nat Prod Res 2021 Mar 1:1-10. Epub 2021 Mar 1.

Fujian Provincial Key Laboratory of Innovative Drug Target, School of Pharmaceutical Sciences, Xiamen University, Xiamen, People's Republic of China.

One undescribed lignan, one new natural product, along with fourteen known compounds, were isolated from the roots of . The structures of the isolates were elucidated by comprehensive spectroscopic technologies, including UV, IR, HRESIMS, and NMR. The absolute configuration of was determined by comparison of experimental and calculated ECD data. The cytotoxicity of all the compounds against HeLa and HepG2 cell lines was evaluated and compound showed considerable cytotoxic effect towards HepG2 cells. Also, the apoptotic effect of on HepG2 cells and the effect of on the key proteins (p-JNK and p-p38) in MAPK (Mitogen-activated protein kinases) pathways were studied by flow cytometry and western blotting experiment. As a result, compound induced the apoptosis of HepG2 cells, and dose-dependently increased the phosphorylation of JNK and p38. Thus, might trigger HepG2 cells apoptosis via JNK/p38 MAPK signaling pathway.
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http://dx.doi.org/10.1080/14786419.2021.1892099DOI Listing
March 2021

Prenylated flavonoids from Ficus hirta induces HeLa cells apoptosis via MAPK and AKT signaling pathways.

Bioorg Med Chem Lett 2021 Apr 18;38:127859. Epub 2021 Feb 18.

Fujian Provincial Key Laboratory of Innovative Drug Target, School of Pharmaceutical Sciences, Xiamen University, Xiamen 361102, People's Republic of China. Electronic address:

A pair of undescribed enantiomers, (±) ficusflavonid A (1a/1b), along with five known analogues, were isolated from the roots of Ficus hirta. Their structures were determined by the analysis of extensive spectroscopic data (including UV, IR, HRESIMS and NMR). Two enantiomers (1a and 1b) were successfully separated by chiral chromatographic column and their absolute configurations were assigned by the comparison of experimental and calculated ECD data. The cytotoxicity of all the isolates against HeLa, MCF-7, HepG2 and H460 cell lines were evaluated by MTT assay. Among them, 4 suppressed the proliferation of HeLa cells with the IC value of 28.88 μM. Furthermore, the apoptotic effect of 4 on HeLa cells and the level of several crucial proteins in AKT/MAPKs signaling pathways were analyzed by flow cytometer and western blot assay. As a result, 4 induced HeLa cell apoptosis in a dose dependent manner and significantly increased the protein levels of p-JNK and p-p38, whereas distinctly reduced the expression of p-AKT, and p-ERK. Thus, compound 4 might induce HeLa cells apoptosis via MAPK and AKT signaling pathways, which could be considered as a potential leading compound for the development of anticancer drugs.
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http://dx.doi.org/10.1016/j.bmcl.2021.127859DOI Listing
April 2021

[Multiple Organ Echinococcosis:Report of One Case and Literature Review].

Zhongguo Yi Xue Ke Xue Yuan Xue Bao 2020 Dec;42(6):840-844

Department of Obstetrics and Gynecology, the First Affiliated Hospital of Xi'an Jiaotong University,Xi'an 710061,China.

A patient with multiple-organ echinococcosis suffered from liver echinococcosis,lung echinococcosis,and pelvic echinococcosis successively in the past three decades.From the first operation at 19 years-old,she underwent operations several times due to the recurrence of multiple organ involvement.Echinococcosis is a zoonotic disease.Although the liver usually is the primary site,the disease can also invade many other organs.Diagnosis is typically based on disease history and imaging findings.Thorough removal of the lesions during the first operation is particularly important.Comprehensive evaluations and multi-disciplinary team are helpful in the treatment of patients with multiple organ invasion.
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http://dx.doi.org/10.3881/j.issn.1000-503X.12807DOI Listing
December 2020

Cytotoxic polyprenylated phloroglucinol derivatives from Hypericum elodeoides Choisy modulating the transactivation of RXRα.

Bioorg Chem 2021 Feb 23;107:104578. Epub 2020 Dec 23.

Fujian Provincial Key Laboratory of Innovative Drug Target, School of Pharmaceutical Sciences, Xiamen University, Xiamen 361005, People's Republic of China. Electronic address:

Hyperelodione D (1), an undescribed polyprenylated phloroglucinol derivative possessing 6/6/5/5 fused tetracyclic core, together with hyperelodiones E-F (2-3), two unreported analogues bearing 6/5/5 fused tricyclic structure, were isolated from Hypericum elodeoides Choisy. Their planar structures were elucidated by spectroscopic analysis (HRESIMS, 1D and 2D NMR) and their absolute configurations were determined by comparison of experimental and calculated ECD data. The cytotoxicity and retinoid X receptor-α (RXRα) related activities of the isolates were evaluated and the plausible biogenetic pathways of 1-3 were proposed.
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http://dx.doi.org/10.1016/j.bioorg.2020.104578DOI Listing
February 2021

Facile Synthesis of Size-Controlled Nitrogen-Doped Mesoporous Carbon Nanosphere Supported Ultrafine Ru Nanoparticles for Selective Hydrogenation of Quinolines.

Chemistry 2020 Dec 18;26(71):17000-17004. Epub 2020 Nov 18.

Key Laboratory of Biofuels, Qingdao Institute of Bioenergy and Bioprocess Technology, Chinese Academy of Sciences, Qingdao, 266101, P. R. China.

Nitrogen-doped mesoporous carbon nanosphere (NMCS) with tunable sizes and uniform mesoporosity was synthesized by a facile soft-templating method. During the synthesis, F127 (PEO-PPO-PEO triblock copolymer) could be used not only as a soft template to generate the mesostructure but also as a size-control agent to tailor the size of NMCS in a relatively wide range of 100 to 700 nm. In addition, the synthesis process was simple and suitable for large-scale production. Moreover, the NMCS was used as support of ultrafine Ru nanoparticles (Ru/NMCS), which exhibited good catalytic performances for selective hydrogenation of quinolones. It is expected that the simple synthetic strategy for the NMCS can generate extensive interest in many catalysis and sorption applications.
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http://dx.doi.org/10.1002/chem.202003492DOI Listing
December 2020

Cytotoxic compound triacremoniate from Marine Fungus Acremonium citrinum. MMF4.

Fitoterapia 2020 Nov 29;147:104766. Epub 2020 Oct 29.

Fujian Provincial Key Laboratory of Innovative Drug Target, School of Pharmaceutical Sciences, Xiamen University, Xiamen 361005, People's Republic of China. Electronic address:

Two new compounds, triacremoniate (1) and dietziamide C (2) along with known compounds β-Adenosine (3) and acrepyrone A (4) were obtained from the mangrove-derived fungus Acremonium citrinum. MMF4. Their structures were unambiguously determined by extensive spectroscopic methods, including UV, IR, HRESIMS and NMR. Triacremoniate (1) can promote apoptosis of HeLa cells by increasing the PARP cleavage and the phosphorylation of JNK and p38.
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http://dx.doi.org/10.1016/j.fitote.2020.104766DOI Listing
November 2020

Chemical Constituents from Endophytic Fungus Annulohypoxylon cf. stygium in Leaves of Anoectochilus roxburghii.

Chem Biodivers 2020 Sep 31;17(9):e2000424. Epub 2020 Aug 31.

Fujian Provincial Key Laboratory of Innovative Drug Target, School of Pharmaceutical Sciences, Xiamen University, Xiamen, 361005, P. R. China.

The chemical investigation on endophytic fungus Annulohypoxylon cf. stygium in leaves of Anoectochilus roxburghii (Wall.) Lindl. has been performed. Sixteen compounds were isolated and their structures were identified as (-)-notoamide A, (-)-notoamide B, (+)-versicolamide B, notoamide C, notoamide D, stephacidin A, sterigmatocystin, dihydrosterigmatocystin, secosterigmatocystin, versiconol, averufanin, kipukasin D, kipukasin E, diorcinal, palmarumycin CP2 and (-)-(3R)-mellein methyl ether, respectively, by spectroscopic analysis and comparison with literature data. All the compounds were isolated from Annulohypoxylon genus for the first time. Sterigmatocystin and palmarumycin CP2 showed selective cytotoxic activities against HepG2, HeLa, MCF-7 and HT-29.
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http://dx.doi.org/10.1002/cbdv.202000424DOI Listing
September 2020

Hollow Carbon Sphere Nanoreactors Loaded with PdCu Nanoparticles: Void-Confinement Effects in Liquid-Phase Hydrogenations.

Angew Chem Int Ed Engl 2020 Oct 18;59(42):18374-18379. Epub 2020 Aug 18.

Key Laboratory of Biofuels, Qingdao Institute of Bioenergy and Bioprocess Technology, Chinese Academy of Sciences, Qingdao, 266101, China.

Nanoreactors with hollow structures have attracted great interest in catalysis research due to their void-confinement effects. However, the challenge in unambiguously unraveling these confinement effects is to decouple them from other factors affecting catalysis. Here, we synthesize a pair of hollow carbon sphere (HCS) nanoreactors with presynthesized PdCu nanoparticles encapsulated inside of HCS ([email protected]) and supported outside of HCS (PdCu/HCS), respectively, while keeping other structural features the same. Based on the two comparative nanoreactors, void-confinement effects in liquid-phase hydrogenation are investigated in a two-chamber reactor. It is found that hydrogenations over [email protected] are shape-selective catalysis, can be accelerated (accumulation of reactants), decelerated (mass transfer limitation), and even inhibited (molecular-sieving effect); conversion of the intermediate in the void space can be further promoted. Using this principle, a specific imine is selectively produced. This work provides a proof of concept for fundamental catalytic action of the hollow nanoreactors.
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http://dx.doi.org/10.1002/anie.202007297DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7590117PMC
October 2020

Resveratrol Counteracts Hypoxia-Induced Gastric Cancer Invasion and EMT through Hedgehog Pathway Suppression.

Anticancer Agents Med Chem 2020 ;20(9):1105-1114

Department of General Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi, China.

Background: Gastric Cancer (GC) is one of the most malignant and lethal tumors worldwide. The hypoxic microenvironment is correlated with GC cell invasion, metastasis and Epithelial-Mesenchymal Transition (EMT). Resveratrol is a compound extracted from various plants, including grapes, berries, and some traditional Chinese medicines. Recently, the anticancer properties of resveratrol against many cancers have been reported in a range of studies. However, the exact mechanism through which resveratrol prevents GC invasion and metastasis under hypoxic conditions remains unclear.

Objective: The objective of this study is to show to what extent resveratrol could inhibit the hypoxia-induced malignant biological behavior of GC.

Methods: SGC-7901 cells were cultured in a consistent 3% O2 hypoxic condition or 21% O2 normal condition for 48 hours to establish an in vitro hypoxia model. Western blot and qRT-PCR were used to detect EMT markers of SGC- 7901 cells, including E-cadherin, HIF-1a, Vimentin, etc. Transwell Matrigel Invasion Assays were used to test the invasive ability of SGC-7901 cells. The siRNA targeting Gli-1 showed its role in hypoxia-induced EMT and invasion of SGC-7901 cells.

Results: Resveratrol was found to significantly decrease HIF-1α protein levels induced by hypoxia in SGC-7901 cells. HIF-1α accumulation was found to promote cell proliferation, migration, and invasive capacities in addition to EMT changes through the activation of the Hedgehog pathway. These effects were found to be reversed by resveratrol.

Conclusion: Therefore, these data indicate that resveratrol may serve as a potential anticancer agent for the treatment of GC, even in a hypoxic tumor microenvironment.
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http://dx.doi.org/10.2174/1871520620666200402080034DOI Listing
May 2021

Phenolic glycosides and flavonoids with antioxidant and anticancer activities from .

Nat Prod Res 2020 Mar 12:1-8. Epub 2020 Mar 12.

Fujian Provincial Key Laboratory of Innovative Drug Target, School of Pharmaceutical Sciences, Xiamen University, Xiamen, People's Republic of China.

Descaudatine A (), an undescribed phenolic glycoside, along with a known analogue () and ten flavonoids (), were isolated from the whole plant of . Compounds and exhibited potent antioxidant activities with the IC of 58.59 μM and 31.31 μM, respectively, which were approached to that of the positive control Vitamin C (IC = 46.32 μM). Meanwhile, showed moderate antioxidant activity with the IC of 173.9 μM. Besides, compounds and inhibited the proliferation of HeLa cells with IC values of 56.14 μM and 69.04 μM, respectively. Further studies indicated that and could dose-dependently induce PARP cleavage and might trigger caspase-3, 8, 9 activation to induce apoptosis. RXRα is an ideal anticancer target of nuclear receptor. The reporter gene assay of RXRα indicated that and could inhibited the 9--RA induced RXRα transcription in a concentration-dependent manner.
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http://dx.doi.org/10.1080/14786419.2020.1739044DOI Listing
March 2020

MicroRNA-1269 promotes cell proliferation via the AKT signaling pathway by targeting RASSF9 in human gastric cancer.

Cancer Cell Int 2019 21;19:308. Epub 2019 Nov 21.

3Department of General Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061 Shaanxi China.

Background: MicroRNAs (miRNAs) play key roles in tumorigenesis and progression of gastric cancer (GC). miR-1269 has been reported to be upregulated in several cancers and plays a crucial role in carcinogenesis and cancer progression. However, the biological function of miR-1269 in human GC and its mechanism remain unclear and need to be further elucidated.

Methods: The expression of miR-1269 in GC tissues and cell lines was detected by quantitative real-time PCR (qRT-PCR). Target prediction programs (TargetScanHuman 7.2 and miRBase) and a dual-luciferase reporter assay were used to confirm that Ras-association domain family 9 (RASSF9) is a target gene of miR-1269. The expression of RASSF9 was measured by qRT-PCR and Western blotting in GC tissues. MTT and cell counting assays were used to explore the effect of miR-1269 on GC cell proliferation. The cell cycle and apoptosis were measured by flow cytometry. RASSF9 knockdown and overexpression were used to further verify the function of the target gene.

Results: We found that miR-1269 expression was upregulated in human GC tissues and cell lines. The overexpression of miR-1269 promoted GC cell proliferation and cell cycle G1-S transition and suppressed apoptosis. The inhibition of miR-1269 inhibited cell growth and G1-S transition and induced apoptosis. miR-1269 expression was inversely correlated with RASSF9 expression in GC tissues. RASSF9 was verified to be a direct target of miR-1269 by using a luciferase reporter assay. The overexpression of miR-1269 decreased RASSF9 expression at both the mRNA and protein levels, and the inhibition of miR-1269 increased RASSF9 expression. Importantly, silencing RASSF9 resulted in the same biological effects in GC cells as those induced by overexpression of miR-1269. Overexpression of RASSF9 reversed the effects of miR-1269 overexpression on GC cells. Both miR-1269 overexpression and RASSF9 silencing activated the AKT signaling pathway, which modulated cell cycle regulators (Cyclin D1 and CDK2). In contrast, inhibition of miR-1269 and RASSF9 overexpression inhibited the AKT signaling pathway. Moreover, miR-1269 and RASSF9 also regulated the Bax/Bcl-2 signaling pathway.

Conclusions: Our results demonstrate that miR-1269 promotes GC cell proliferation and cell cycle G1-S transition by activating the AKT signaling pathway and inhibiting cell apoptosis via regulation of the Bax/Bcl-2 signaling pathway by targeting RASSF9. Our findings indicate an oncogenic role of miR-1269 in GC pathogenesis and the potential use of miR-1269 in GC therapy.
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http://dx.doi.org/10.1186/s12935-019-1026-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6873743PMC
November 2019

RWHMDA: Random Walk on Hypergraph for Microbe-Disease Association Prediction.

Front Microbiol 2019 10;10:1578. Epub 2019 Jul 10.

Academy of Mathematics and Systems Science, Chinese Academy of Sciences, Beijing, China.

Based on advancements in deep sequencing technology and microbiology, increasing evidence indicates that microbes inhabiting humans modulate various host physiological phenomena, thus participating in various disease pathogeneses. Owing to increasing availability of biological data, further studies on the establishment of efficient computational models for predicting potential associations are required. In particular, computational approaches can also reduce the discovery cycle of novel microbe-disease associations and further facilitate disease treatment, drug design, and other scientific activities. This study aimed to develop a model based on the random walk on hypergraph for microbe-disease association prediction (RWHMDA). As a class of higher-order data representation, hypergraph could effectively recover information loss occurring in the normal graph methodology, thus exclusively illustrating multiple pair-wise associations. Integrating known microbe-disease associations in the Human Microbe-Disease Association Database (HMDAD) and the Gaussian interaction profile kernel similarity for microbes, random walk was then implemented for the constructed hypergraph. Consequently, RWHMDA performed optimally in predicting the underlying disease-associated microbes. More specifically, our model displayed AUC values of 0.8898 and 0.8524 in global and local leave-one-out cross-validation (LOOCV), respectively. Furthermore, three human diseases (asthma, Crohn's disease, and type 2 diabetes) were studied to further illustrate prediction performance. Moreover, 8, 10, and 8 of the 10 highest ranked microbes were confirmed through recent experimental or clinical studies. In conclusion, RWHMDA is expected to display promising potential to predict disease-microbe associations for follow-up experimental studies and facilitate the prevention, diagnosis, treatment, and prognosis of complex human diseases.
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http://dx.doi.org/10.3389/fmicb.2019.01578DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6635699PMC
July 2019

Steroids from the Deep-Sea-Derived Fungus MCCC 3A00475 Induced Apoptosis via Retinoid X Receptor ()-α Pathway.

Mar Drugs 2019 Mar 19;17(3). Epub 2019 Mar 19.

School of Pharmaceutical Sciences, Xiamen University, South Xiangan Road, Xiamen 361005, China.

Five new ergostanes, penicisteroids D-H (-), were isolated from the liquid culture of the deep-sea-derived fungus MCCC 3A00475, along with 27 known compounds. The structures of the new steroids were established mainly on the basis of extensive analysis of 1D and 2D NMR as well as HRESIMS data. Moreover, the absolute configurations of were confirmed unambiguously by the single-crystal X-ray crystallography. Compounds and ⁻ showed moderate antiproliferative effects selectively against 12 different cancer cell lines with IC values of around 5 μM. Compounds and , potent binders with Kd values of 13.8 and 12.9 μM, respectively, could induce apoptosis by a Retinoid X Receptor ()--dependent mechanism by regulating RXRα transcriptional expression and promoting the poly-ADP-ribose polymerase (PARP) cleavage. Moreover, they could inhibit proliferation by cell cycle arrest at the G0/G1 phase.
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http://dx.doi.org/10.3390/md17030178DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6472029PMC
March 2019

Secondary metabolites of petri-dish cultured Antrodia camphorata and their hepatoprotective activities against alcohol-induced liver injury in mice.

Chin J Nat Med 2019 Jan;17(1):33-42

Fujian Provincial Key Laboratory of Innovative Drug Target, School of Pharmaceutical Sciences, Xiamen University, Xiamen 361005, China. Electronic address:

Antrodia camphorata, a well-known and highly valued edible medicinal mushroom with intriguing activities like liver protection, has been traditionally used for the treatment of alcoholic liver disease. A. camphorata shows highly medicinal and commercial values with the demand far exceeds the available supply. Thus, the petri-dish cultured A. camphorata (PDCA) is expected to develope as a substitute. In this paper, nineteen triterpenes were isolated from PDCA, and thirteen of them were the unique anthroic acids in A. camphorata, including the main content antcin K, which suggested that PDCA produced a large array of the same anthroic acids as the wild one. Furthermore, no obvious acute toxicity was found suggesting the edible safety of PDCA. In mice alcohol-induced liver injury model, triglyceride (TG), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) had been reduced by the PDCA powder as well as the main content antcin K, which indicated that the PDCA could protect alcoholic liver injury in mice model and antcin K could be the effective component responsible for the hepatoprotective activities of PDCA against alcoholic liver diseases.
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http://dx.doi.org/10.1016/S1875-5364(19)30007-XDOI Listing
January 2019

Integrating random walk and binary regression to identify novel miRNA-disease association.

BMC Bioinformatics 2019 Jan 28;20(1):59. Epub 2019 Jan 28.

School of Information and Control Engineering, China University of Mining and Technology, No.1, Daxue Road, Xuzhou, 221116, Jiangsu, China.

Background: In the last few decades, cumulative experimental researches have witnessed and verified the important roles of microRNAs (miRNAs) in the development of human complex diseases. Benefitting from the rapid growth both in the availability of miRNA-related data and the development of various analysis methodologies, up until recently, some computational models have been developed to predict human disease related miRNAs, efficiently and quickly.

Results: In this work, we proposed a computational model of Random Walk and Binary Regression-based MiRNA-Disease Association prediction (RWBRMDA). RWBRMDA extracted features for each miRNA from random walk with restart on the integrated miRNA similarity network for binary logistic regression to predict potential miRNA-disease associations. RWBRMDA obtained AUC of 0.8076 in the leave-one-out cross validation. Additionally, we carried out three different patterns of case studies on four human complex diseases. Specifically, Esophageal cancer and Prostate cancer were conducted as one kind of case study based on known miRNA-disease associations in HMDD v2.0 database. Out of the top 50 predicted miRNAs, 94 and 90% were respectively confirmed by recent experimental reports. To simulate new disease without known related miRNAs, the information of known Breast cancer related miRNAs was removed. As a result, 98% of the top 50 predicted miRNAs for Breast cancer were confirmed. Lymphoma, the verified ratio of which was 88%, was used to assess the prediction robustness of RWBRMDA based on the association records in HMDD v1.0 database.

Conclusions: We anticipated that RWBRMDA could benefit the future experimental investigations about the relation between human disease and miRNAs by generating promising and testable top-ranked miRNAs, and significantly reducing the effort and cost of identification works.
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http://dx.doi.org/10.1186/s12859-019-2640-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6350368PMC
January 2019

Coding mutations in contribute to Parkinson's disease.

Proc Natl Acad Sci U S A 2018 11 22;115(45):11567-11572. Epub 2018 Oct 22.

Department of Pharmacology, Soochow University, College of Pharmaceutical Sciences, 215021 Suzhou, China.

Whole-exome sequencing has been successful in identifying genetic factors contributing to familial or sporadic Parkinson's disease (PD). However, this approach has not been applied to explore the impact of de novo mutations on PD pathogenesis. Here, we sequenced the exomes of 39 early onset patients, their parents, and 20 unaffected siblings to investigate the effects of de novo mutations on PD. We identified 12 genes with de novo mutations (, , , , , , , , , , , and ), which could be functionally relevant to PD pathogenesis. Further analyses of two independent case-control cohorts (1,852 patients and 1,565 controls in one cohort and 3,237 patients and 2,858 controls in the other) revealed that harbors significantly more rare nonsynonymous variants ( = 1.01E-5, odds ratio = 11.3) in PD patients than in controls. Functional studies in demonstrated that the loss of could reduce the climbing ability, dopamine level, and number of dopaminergic neurons in 30-day-old flies and could induce apoptosis in fly brain. Together, our data suggest that de novo mutations could contribute to early onset PD pathogenesis and identify as a candidate gene for PD.
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http://dx.doi.org/10.1073/pnas.1809969115DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6233099PMC
November 2018

Maximal entropy random walk on heterogenous network for MIRNA-disease Association prediction.

Math Biosci 2018 12 16;306:1-9. Epub 2018 Oct 16.

Academy of Mathematics and Systems Science, Chinese Academy of Sciences, Beijing 100190, China.

The last few decades have verified the vital roles of microRNAs in the development of human diseases and witnessed the increasing interest in the prediction of potential disease-miRNA associations. Owning to the open access of many miRNA-related databases, up until recently, kinds of feasible in silico models have been proposed. In this work, we developed a computational model of Maximal Entropy Random Walk on heterogenous network for MiRNA-disease Association prediction (MERWMDA). MERWMDA integrated known disease-miRNA association, pair-wise functional relation of miRNAs and pair-wise semantic relation of diseases into a heterogenous network comprised of disease and miRNA nodes full of information. As a kind of widely-applied biased walk process with more randomness, MERW was then implemented on the heterogenous network to reveal potential disease-miRNA associations. Cross validation was further performed to evaluate the performance of MERWMDA. As a result, MERWMDA obtained AUCs of 0.8966 and 0.8491 respectively in the aspect of global and local leave-one-out cross validation. What' more, three different case study strategies on four human complex diseases were conducted to comprehensively assess the quality of the model. Specifically, one kind of case study on Esophageal cancer and Prostate cancer were conducted based on HMDD v2.0 database. 94% and 88% out of the top 50 ranked miRNAs were confirmed by recent literature, respectively. To simulate new disease without known related miRNAs, Lung cancer (confirmed ratio 94%) associated miRNAs were removed for case study. Lymphoma (verified ratio 88%) was adopted to assess the prediction robustness of MERWMDA based on HMDD v1.0 database. We anticipated that MERWMDA could offer valuable candidates for in vitro biomedical experiments in future.
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http://dx.doi.org/10.1016/j.mbs.2018.10.004DOI Listing
December 2018

Pharmacological activation of REV-ERBα represses LPS-induced microglial activation through the NF-κB pathway.

Acta Pharmacol Sin 2019 Jan 27;40(1):26-34. Epub 2018 Jun 27.

Laboratory of Molecular Neuropathology, Jiangsu Key Laboratory of Translational Research and Therapy for Neuropsychiatric Disorders & Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, 215123, China.

REV-ERBα, the NR1D1 (nuclear receptor subfamily 1, group D, member 1) gene product, is a dominant transcriptional silencer that represses the expression of genes involved in numerous physiological functions, including circadian rhythm, inflammation, and metabolism, and plays a crucial role in maintaining immune functions. Microglia-mediated neuroinflammation is tightly associated with various neurodegenerative diseases and psychiatric disorders. However, the role of REV-ERBα in neuroinflammation is largely unclear. In this study, we investigated whether and how pharmacological activation of REV-ERBα affected lipopolysaccharide (LPS)-induced neuroinflammation in mouse microglia in vitro and in vivo. In BV2 cells or primary mouse cultured microglia, application of REV-ERBα agonist GSK4112 or SR9011 dose-dependently suppressed LPS-induced microglial activation through the nuclear factor kappa B (NF-κB) pathway. In BV2 cells, pretreatment with GSK4112 inhibited LPS-induced phosphorylation of the inhibitor of NF-κB alpha (IκBα) kinase (IκK), thus restraining the phosphorylation and degradation of IκBα, and blocked the nuclear translocation of p65, a NF-κB subunit, thereby suppressing the expression and secretion of the proinflammatory cytokines, such as interleukin 6 (IL-6) and tumor necrosis factor α (TNFα). Moreover, REV-ERBα agonist-induced inhibition on neuroinflammation protected neurons from microglial activation-induced damage, which were also demonstrated in mice with their ventral midbrain microinjected with GSK4112, and then stimulated with LPS. Our results reveal that enhanced REV-ERBα activity suppresses microglial activation through the NF-κB pathway in the central nervous system.
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http://dx.doi.org/10.1038/s41401-018-0064-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6318300PMC
January 2019

A strategy to find novel candidate anti-Alzheimer's disease drugs by constructing interaction networks between drug targets and natural compounds in medical plants.

PeerJ 2018 11;6:e4756. Epub 2018 May 11.

State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China.

Background: Alzheimer' disease (AD) is an ultimately fatal degenerative brain disorder that has an increasingly large burden on health and social care systems. There are only five drugs for AD on the market, and no new effective medicines have been discovered for many years. Chinese medicinal plants have been used to treat diseases for thousands of years, and screening herbal remedies is a way to develop new drugs.

Methods: We used molecular docking to screen 30,438 compounds from Traditional Chinese Medicine (TCM) against a comprehensive list of AD target proteins. TCM compounds in the top 0.5% of binding affinity scores for each target protein were selected as our research objects. Structural similarities between existing drugs from DrugBank database and selected TCM compounds as well as the druggability of our candidate compounds were studied. Finally, we searched the CNKI database to obtain studies on anti-AD Chinese plants from 2007 to 2017, and only clinical studies were included.

Results: A total of 1,476 compounds (top 0.5%) were selected as drug candidates. Most of these compounds are abundantly found in plants used for treating AD in China, especially the plants from two genera Panax and Morus. We classified the compounds by single target and multiple targets and analyzed the interactions between target proteins and compounds. Analysis of structural similarity revealed that 17 candidate anti-AD compounds were structurally identical to 14 existing approved drugs. Most of them have been reported to have a positive effect in AD. After filtering for compound druggability, we identified 11 anti-AD compounds with favorable properties, seven of which are found in anti-AD Chinese plants. Of 11 anti-AD compounds, four compounds 5,862, 5,863, 5,868, 5,869 have anti-inflammatory activity. The compound 28,814 mainly has immunoregulatory activity. The other six compounds have not yet been reported for any biology activity at present.

Discussion: Natural compounds from TCM provide a broad prospect for the screening of anti-AD drugs. In this work, we established networks to systematically study the connections among natural compounds, approved drugs, TCM plants and AD target proteins with the goal of identifying promising drug candidates. We hope that our study will facilitate in-depth research for the treatment of AD in Chinese medicine.
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http://dx.doi.org/10.7717/peerj.4756DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5951129PMC
May 2018

MKRMDA: multiple kernel learning-based Kronecker regularized least squares for MiRNA-disease association prediction.

J Transl Med 2017 Dec 12;15(1):251. Epub 2017 Dec 12.

Academy of Mathematics and Systems Science, Chinese Academy of Sciences, Beijing, 100190, China.

Background: Recently, as the research of microRNA (miRNA) continues, there are plenty of experimental evidences indicating that miRNA could be associated with various human complex diseases development and progression. Hence, it is necessary and urgent to pay more attentions to the relevant study of predicting diseases associated miRNAs, which may be helpful for effective prevention, diagnosis and treatment of human diseases. Especially, constructing computational methods to predict potential miRNA-disease associations is worthy of more studies because of the feasibility and effectivity.

Methods: In this work, we developed a novel computational model of multiple kernels learning-based Kronecker regularized least squares for MiRNA-disease association prediction (MKRMDA), which could reveal potential miRNA-disease associations by automatically optimizing the combination of multiple kernels for disease and miRNA.

Results: MKRMDA obtained AUCs of 0.9040 and 0.8446 in global and local leave-one-out cross validation, respectively. Meanwhile, MKRMDA achieved average AUCs of 0.8894 ± 0.0015 in fivefold cross validation. Furthermore, we conducted three different kinds of case studies on some important human cancers for further performance evaluation. In the case studies of colonic cancer, esophageal cancer and lymphoma based on known miRNA-disease associations in HMDDv2.0 database, 76, 94 and 88% of the corresponding top 50 predicted miRNAs were confirmed by experimental reports, respectively. In another two kinds of case studies for new diseases without any known associated miRNAs and diseases only with known associations in HMDDv1.0 database, the verified ratios of two different cancers were 88 and 94%, respectively.

Conclusions: All the results mentioned above adequately showed the reliable prediction ability of MKRMDA. We anticipated that MKRMDA could serve to facilitate further developments in the field and the follow-up investigations by biomedical researchers.
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http://dx.doi.org/10.1186/s12967-017-1340-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5727873PMC
December 2017

Dendritic cell nuclear protein-1 regulates melatonin biosynthesis by binding to BMAL1 and inhibiting the transcription of N-acetyltransferase in C6 cells.

Acta Pharmacol Sin 2018 Apr 7;39(4):597-606. Epub 2017 Dec 7.

Laboratory of Molecular Neuropathology, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China.

Dendritic cell nuclear protein-1 (DCNP1) is a protein associated with major depression. In the brains of depression patients, DCNP1 is up-regulated. However, how DCNP1 participates in the pathogenesis of major depression remains unknown. In this study, we first transfected HEK293 cells with EGFP-DCNP1 and demonstrated that the full-length DCNP1 protein was localized in the nucleus, and RRK (the residues 117-119) composed its nuclear localization signal (NLS). An RRK-deletion form of DCNP1 (DCNP1) and truncated form (DCNP1), each lacking the RRK residues, did not show the specific nuclear localization like full-length DCNP1 in the cells. A rat glioma cell line C6 can synthesize melatonin, a hormone that plays important roles in both sleep and depression. We then revealed that transfection of C6 cells with full-length DCNP1 but not DCNP1 or DCNP1 significantly decreased the levels of melatonin. Furthermore, overexpression of full-length DCNP1, but not DCNP1 or DCNP1, in C6 cells significantly decreased both the mRNA and protein levels of N-acetyltransferase (NAT), a key enzyme in melatonin synthesis. Full-length DCNP1 but not DCNP1 or DCNP1 was detected to interact with the Nat promoter and inhibited its activity through its E-box motif. Furthermore, full-length DCNP1 but not the mutants interacted with and repressed the transcriptional activity of BMAL1, a transcription factor that transactivates Nat through the E-box motif. In conclusion, we have shown that RRK (the residues 117-119) are the NLS responsible for DCNP1 nuclear localization. Nuclear DCNP1 represses NAT expression and melatonin biosynthesis by interacting with BMAL1 and repressing its transcriptional activity. Our study reveals a connection between the major depression candidate protein DCNP1, circadian system and melatonin biosynthesis, which may contribute to the pathogenesis of depression.
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http://dx.doi.org/10.1038/aps.2017.163DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5888688PMC
April 2018

Serum Response Factor Promotes Dopaminergic Neuron Survival via Activation of Beclin 1-Dependent Autophagy.

Neuroscience 2018 02 28;371:288-295. Epub 2017 Nov 28.

Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China; Institute of Neuroscience, Soochow University, Suzhou 215123, China. Electronic address:

Serum response factor (SRF), a transcription factor highly expressed in neurons, is involved in neuronal survival and the pathogenesis of some neurodegenerative disorders. The ablation of SRF renders the midbrain dopaminergic (DA) neurons vulnerable to 1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine-induced neurotoxicity, however, the underlying mechanisms remain poorly understood. Here, we report decreased SRF levels in the substantia nigra (SN) of rotenone-treated rats that was associated with the loss of tyrosine hydroxylase (TH)-positive neurons. SRF expression was also reduced in rotenone-treated PC12 cells in vitro. In addition, Srf knockdown augmented rotenone-induced toxicity in PC12 cells. In contrast, overexpression of Srf attenuated the cells' sensitivity to rotenone and alleviated rotenone-induced α-synuclein accumulation. The protective effect of SRF was abolished when the expression of autophagy-related proteins Beclin 1 and Atg5 was suppressed. These results suggested that SRF may promote DA neuron survival by regulating autophagy, and thus serves as a critical molecule in PD progression.
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http://dx.doi.org/10.1016/j.neuroscience.2017.11.040DOI Listing
February 2018

HAMDA: Hybrid Approach for MiRNA-Disease Association prediction.

J Biomed Inform 2017 Dec 31;76:50-58. Epub 2017 Oct 31.

Academy of Mathematics and Systems Science, Chinese Academy of Sciences, Beijing 100190, China.

For decades, enormous experimental researches have collectively indicated that microRNA (miRNA) could play indispensable roles in many critical biological processes and thus also the pathogenesis of human complex diseases. Whereas the resource and time cost required in traditional biology experiments are expensive, more and more attentions have been paid to the development of effective and feasible computational methods for predicting potential associations between disease and miRNA. In this study, we developed a computational model of Hybrid Approach for MiRNA-Disease Association prediction (HAMDA), which involved the hybrid graph-based recommendation algorithm, to reveal novel miRNA-disease associations by integrating experimentally verified miRNA-disease associations, disease semantic similarity, miRNA functional similarity, and Gaussian interaction profile kernel similarity into a recommendation algorithm. HAMDA took not only network structure and information propagation but also node attribution into consideration, resulting in a satisfactory prediction performance. Specifically, HAMDA obtained AUCs of 0.9035 and 0.8395 in the frameworks of global and local leave-one-out cross validation, respectively. Meanwhile, HAMDA also achieved good performance with AUC of 0.8965 ± 0.0012 in 5-fold cross validation. Additionally, we conducted case studies about three important human cancers for performance evaluation of HAMDA. As a result, 90% (Lymphoma), 86% (Prostate Cancer) and 92% (Kidney Cancer) of top 50 predicted miRNAs were confirmed by recent experiment literature, which showed the reliable prediction ability of HAMDA.
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http://dx.doi.org/10.1016/j.jbi.2017.10.014DOI Listing
December 2017

Modulation of the Nur77-Bcl-2 apoptotic pathway by p38α MAPK.

Oncotarget 2017 Sep 13;8(41):69731-69745. Epub 2017 Jul 13.

School of Pharmaceutical Sciences, Fujian Provincial Key Laboratory of Innovative Drug Target Research, Xiamen University, Xiamen, China.

Orphan nuclear receptor Nur77 promotes apoptosis by targeting mitochondria through interaction with Bcl-2, an event that converts Bcl-2 from a survival to killer. However, how the Nur77-Bcl-2 apoptotic pathway is regulated remains largely unknown. In this study, we examined the regulation of the Nur77-Bcl-2 pathway by CCE9, a xanthone compound. Our results demonstrated that the apoptotic effect of CCE9 depended on its induction of Nur77 expression, cytoplasmic localization, and mitochondrial targeting. The activation of the Nur77-Bcl-2 pathway by CCE9 was associated with its activation of p38α MAPK. Inhibition of p38α MAPK activation by knocking down or knocking out p38α MAPK impaired the effect of CCE9 on inducing apoptosis and the expression and cytoplasmic localization of Nur77. In addition, CCE9 activation of p38α MAPK resulted in Bcl-2 phosphorylation and Bcl-2 interaction with Nur77, whereas inhibition of p38α MAPK activation or expression suppressed the interaction. Moreover, mutating Ser87 and Thr56 in the loop of Bcl-2, which are known to be phosphorylated by p38α MAPK, impaired the ability Bcl-2 to interact with Nur77. Together, our results reveal a profound role of p38α MAPK in regulating the Nur77-Bcl-2 apoptotic pathway through its modulation of Nur77 expression, Bcl-2 phosphorylation, and their interaction.
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http://dx.doi.org/10.18632/oncotarget.19227DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5642512PMC
September 2017

Catalysis Meets Nonthermal Separation for the Production of (Alkyl)phenols and Hydrocarbons from Pyrolysis Oil.

Angew Chem Int Ed Engl 2017 02 27;56(9):2334-2339. Epub 2017 Jan 27.

Max-Planck-Institut für Kohlenforschung, 45470, Mülheim an der Ruhr, Germany.

A simple and efficient hydrodeoxygenation strategy is described to selectively generate and separate high-value alkylphenols from pyrolysis bio-oil, produced directly from lignocellulosic biomass. The overall process is efficient and only requires low pressures of hydrogen gas (5 bar). Initially, an investigation using model compounds indicates that MoC /C is a promising catalyst for targeted hydrodeoxygenation, enabling selective retention of the desired Ar-OH substituents. By applying this procedure to pyrolysis bio-oil, the primary products (phenol/4-alkylphenols and hydrocarbons) are easily separable from each other by short-path column chromatography, serving as potential valuable feedstocks for industry. The strategy requires no prior fractionation of the lignocellulosic biomass, no further synthetic steps, and no input of additional (e.g., petrochemical) platform molecules.
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http://dx.doi.org/10.1002/anie.201610405DOI Listing
February 2017

Activation of Nur77 in microglia attenuates proinflammatory mediators production and protects dopaminergic neurons from inflammation-induced cell death.

J Neurochem 2017 02 21;140(4):589-604. Epub 2016 Dec 21.

Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu, China.

Microglia-mediated neuroinflammation plays a critical role in the pathological development of Parkinson's disease (PD). Orphan nuclear receptor Nur77 (Nur77) is abundant in neurons, while its role in microglia-mediated neuroinflammation remains unclear. The present data demonstrated that the expression of Nur77 in microglia was reduced accompanied by microglia activation in response to lipopolysaccharide (LPS) in vitro and in experimental 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-PD mouse model. Nur77 over-expression or application of Nur77 agonist cytosporone B suppressed the expression of proinflammatory genes, such as inducible nitric oxide NOS, cyclooxygenase-2, IL-1β, and tumor necrosis factor-α in the activated microglia, while silenced Nur77 exaggerated the inflammatory responses in microglia. Moreover, activation of Nur77 suppressed the LPS-induced NF-κB activation which was partly dependent on p38 MAPK activity, since inhibition of p38 MAPK by SB203580 abolished the LPS-activated NF-κB in microglia. On the other hand, inhibition of p38 MAPK attenuated LPS-induced Nur77 reduction. Furthermore, in a microglia-conditioned cultured media system, Nur77 ameliorated the cytotoxicity to MN9D dopaminergic cells. Lastly, cytosporone B attenuated microglia activation and loss of dopaminergic neuron in the substantia nigra pars compacta (SNpc) of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-PD mouse model. Taken together, these findings revealed the first evidence that Nur77 was an important modulator in microglia function that associated with microglia-mediated dopaminergic neurotoxicity, and thus modulation of Nur77 may represent a potential novel target for treatment for neurodegenerative disease.
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http://dx.doi.org/10.1111/jnc.13907DOI Listing
February 2017

Hollow Nano- and Microstructures as Catalysts.

Chem Rev 2016 Nov 7;116(22):14056-14119. Epub 2016 Oct 7.

Department of Heterogeneous Catalysis, Max-Planck-Institut für Kohlenforschung, Kaiser-Wilhelm-Platz 1 , D-45470 Mülheim an der Ruhr, Germany.

Catalysis is at the core of almost every established and emerging chemical process and also plays a central role in the quest for novel technologies for the sustainable production and conversion of energy. Particularly since the early 2000s, a great surge of interest exists in the design and application of micro- and nanometer-sized materials with hollow interiors as solid catalysts. This review provides an updated and critical survey of the ever-expanding material architectures and applications of hollow structures in all branches of catalysis, including bio-, electro-, and photocatalysis. First, the main synthesis strategies toward hollow materials are succinctly summarized, with emphasis on the (regioselective) incorporation of various types of catalytic functionalities within their different subunits. The principles underlying the scientific and technological interest in hollow materials as solid catalysts, or catalyst carriers, are then comprehensively reviewed. Aspects covered include the stabilization of catalysts by encapsulation, the introduction of molecular sieving or stimuli-responsive "auxiliary" functionalities, as well as the single-particle, spatial compartmentalization of various catalytic functions to create multifunctional (bio)catalysts. Examples are also given on the applications which hollow structures find in the emerging fields of electro- and photocatalysis, particularly in the context of the sustainable production of chemical energy carriers. Finally, a critical perspective is provided on the plausible evolution lines for this thriving scientific field, as well as the main practical challenges relevant to the reproducible and scalable synthesis and utilization of hollow micro- and nanostructures as solid catalysts.
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http://dx.doi.org/10.1021/acs.chemrev.6b00374DOI Listing
November 2016

Vitamin K2 suppresses rotenone-induced microglial activation in vitro.

Acta Pharmacol Sin 2016 Sep 8;37(9):1178-89. Epub 2016 Aug 8.

Laboratory of Molecular Neuropathology, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou 215021, China.

Aim: Increasing evidence has shown that environmental factors such as rotenone and paraquat induce neuroinflammation, which contributes to the pathogenesis of Parkinson's disease (PD). In this study, we investigated the molecular mechanisms underlying the repression by menaquinone-4 (MK-4), a subtype of vitamin K2, of rotenone-induced microglial activation in vitro.

Methods: A microglial cell line (BV2) was exposed to rotenone (1 μmol/L) with or without MK-4 treatment. The levels of TNF-α or IL-1β in 100 μL of cultured media of BV2 cells were measured using ELISA kits. BV2 cells treated with rotenone with or without MK4 were subjected to mitochondrial membrane potential, ROS production, immunofluorescence or immunoblot assays. The neuroblastoma SH-SY5Y cells were treated with conditioned media (CM) of BV2 cells that were exposed to rotenone with or without MK-4 treatment, and the cell viability was assessed using MTT assay.

Results: In rotenone-treated BV2 cells, MK-4 (0.5-20 μmol/L) dose-dependently suppressed the upregulation in the expression of iNOS and COX-2 in the cells, as well as the production of TNF-α and IL-1β in the cultured media. MK-4 (5-20 μmol/L) significantly inhibited rotenone-induced nuclear translocation of NF-κB in BV2 cells. MK-4 (5-20 μmol/L) significantly inhibited rotenone-induced p38 activation, ROS production, and caspase-1 activation in BV2 cells. MK-4 (5-20 μmol/L) also restored the mitochondrial membrane potential that had been damaged by rotenone. Exposure to CM from rotenone-treated BV2 cells markedly decreased the viability of SH-SY5Y cells. However, this rotenone-activated microglia-mediated death of SH-SY5Y cells was significantly attenuated when the BV2 cells were co-treated with MK-4 (5-20 μmol/L).

Conclusion: Vitamin K2 can directly suppress rotenone-induced activation of microglial BV2 cells in vitro by repressing ROS production and p38 activation.
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http://dx.doi.org/10.1038/aps.2016.68DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5022102PMC
September 2016

Co3 O4 Nanoparticles Supported on Mesoporous Carbon for Selective Transfer Hydrogenation of α,β-Unsaturated Aldehydes.

Angew Chem Int Ed Engl 2016 09 28;55(37):11101-5. Epub 2016 Jul 28.

Max-Planck-Institut für Kohlenforschung, 45470, Mülheim an der Ruhr, Germany.

A simple and scalable method for synthesizing Co3 O4 nanoparticles supported on the framework of mesoporous carbon (MC) was developed. Benefiting from an ion-exchange process during the preparation, the cobalt precursor is introduced into a mesostructured polymer framework that results in Co3 O4 nanoparticles (ca. 3 nm) supported on MC (Co3 O4 /MC) with narrow particle size distribution and homogeneous dispersion after simple reduction/pyrolysis and mild oxidation steps. The as-obtained Co3 O4 /MC is a highly efficient catalyst for transfer hydrogenation of α,β-unsaturated aldehydes. Selectivities towards unsaturated alcohols are always higher than 95 % at full conversion. In addition, the Co3 O4 /MC shows high stability under the reaction conditions, it can be recycled at least six times without loss of activity.
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http://dx.doi.org/10.1002/anie.201604673DOI Listing
September 2016