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Your search keyword '"Xia, Zhengyuan"' showing total 29 results
Start Over Author "Xia, Zhengyuan" Journal oxidative medicine and cellular longevity
29 results on '"Xia, Zhengyuan"'

1. CXCR4/CX43 Regulate Diabetic Neuropathic Pain via Intercellular Interactions between Activated Neurons and Dysfunctional Astrocytes during Late Phase of Diabetes in Rats and the Effects of Antioxidant N-Acetyl-L-Cysteine

Author

Zhu, Dan, primary, Fan, Tingting, additional, Chen, Yaohua, additional, Huo, Xingyue, additional, Li, Yuping, additional, Liu, Danyong, additional, Cai, Yin, additional, Cheung, Chi Wai, additional, Tang, Jing, additional, Cui, Jian, additional, and Xia, Zhengyuan, additional

Published
2022
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5. Dynamic Patterns of N6-Methyladenosine Profiles of Messenger RNA Correlated with the Cardiomyocyte Regenerability during the Early Heart Development in Mice

Author

Yang, Yuhui, primary, Shen, Siman, additional, Cai, Yin, additional, Zeng, Kejun, additional, Liu, Keyu, additional, Li, Simeng, additional, Zeng, Lanfen, additional, Chen, Linming, additional, Tang, Jing, additional, Hu, Zhe, additional, Xia, Zhengyuan, additional, and Zhang, Liangqing, additional

Published
2021
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28. Cox-2 Inhibition Protects against Hypoxia/Reoxygenation-Induced Cardiomyocyte Apoptosis via Akt-Dependent Enhancement of iNOS Expression.

Author

Pang L, Cai Y, Tang EH, Yan D, Kosuru R, Li H, Irwin MG, Ma H, and Xia Z

Subjects
Apoptosis, Cell Hypoxia, Proto-Oncogene Proteins c-akt metabolism, Signal Transduction, Cyclooxygenase 2 Inhibitors pharmacology, Myocytes, Cardiac drug effects, Nitric Oxide Synthase Type II metabolism
Abstract

The present study explored the potential causal link between ischemia-driven cyclooxygenase-2 (COX-2) expression and enhanced apoptosis during myocardial ischemia/reperfusion (I/R) by using H9C2 cardiomyocytes and primary rat cardiomyocytes subjected to hypoxia/reoxygenation (H/R). The results showed that H/R resulted in higher COX-2 expression than that of controls, which was prevented by pretreatment with Helenalin (NF κ B specific inhibitor). Furthermore, pretreatment with NS398 (COX-2 specific inhibitor) significantly attenuated H/R-induced cell injury [lower lactate dehydrogenase (LDH) leakage and enhanced cell viability] and apoptosis (higher Bcl2 expression and lower level of cleaved caspases-3 and TUNEL-positive cells) in cardiomyocytes. The amelioration of posthypoxic apoptotic cell death was paralleled by significant attenuation of H/R-induced increases in proinflammatory cytokines [interleukin 6 (IL6) and tumor necrosis factor (TNF α )] and reactive oxygen species (ROS) production and by higher protein expression of phosphorylated Akt and inducible nitric oxide synthase (iNOS) and enhanced nitric oxide production. Moreover, the application of LY294002 (Akt-specific inhibitor) or 1400W (iNOS-selective inhibitor) cancelled the cellular protective effects of NS398. Findings from the current study suggest that activation of NF κ B during cardiomyocyte H/R induces the expression of COX-2 and that higher COX-2 expression during H/R exacerbates cardiomyocyte H/R injury via mechanisms that involve cross talks among inflammation, ROS, and Akt/iNOS/NO signaling.

Published
2016
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29. Nitroglycerine-induced nitrate tolerance compromises propofol protection of the endothelial cells against TNF-α: the role of PKC-β2 and NADPH oxidase.

Author

Lei S, Su W, Liu H, Xu J, Xia ZY, Yang QJ, Qiao X, Du Y, Zhang L, and Xia Z

Subjects
Apoptosis drug effects, Cell Survival drug effects, Cytoprotection drug effects, Flow Cytometry, Human Umbilical Vein Endothelial Cells cytology, Human Umbilical Vein Endothelial Cells drug effects, Humans, L-Lactate Dehydrogenase metabolism, Malondialdehyde metabolism, Nitrites metabolism, Phthalimides pharmacology, Superoxides metabolism, Tyrosine analogs & derivatives, Tyrosine metabolism, Human Umbilical Vein Endothelial Cells enzymology, NADPH Oxidases metabolism, Nitrates pharmacology, Nitroglycerin pharmacology, Propofol pharmacology, Protein Kinase C beta metabolism, Tumor Necrosis Factor-alpha pharmacology
Abstract

Continuous treatment with organic nitrates causes nitrate tolerance and endothelial dysfunction, which is involved with protein kinase C (PKC) signal pathway and NADPH oxidase activation. We determined whether chronic administration with nitroglycerine compromises the protective effects of propofol against tumor necrosis factor (TNF-) induced toxicity in endothelial cells by PKC- β2 dependent NADPH oxidase activation. Primary cultured human umbilical vein endothelial cells were either treated or untreated with TNF- α (40 ng/mL) alone or in the presence of the specific PKC- β2 inhibitor CGP53353 (1 μM)), nitroglycerine (10 μM), propofol (100 μM), propofol plus nitroglycerin, or CGP53353 plus nitroglycerine, respectively, for 24 hours. TNF-α increased the levels of superoxide, Nox (nitrate and nitrite), malondialdehyde, and nitrotyrosine production, accompanied by increased protein expression of p-PKC-β2, gP91phox, and endothelial cell apoptosis, whereas all these changes were further enhanced by nitroglycerine. CGP53353 and propofol, respectively, reduced TNF-α induced oxidative stress and cell toxicity. CGP53353 completely prevented TNF- α induced oxidative stress and cell toxicity in the presence or absence of nitroglycerine, while the protective effects of propofol were neutralized by nitroglycerine. It is concluded that nitroglycerine comprises the protective effects of propofol against TNF-α stimulation in endothelial cells, primarily through PKC-β2 dependent NADPH oxidase activation.

Published
2013
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