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第六届国际脑血管病高峰论坛

作者： Guo DJ,Chen YH,Zhao YB~* Department of Neurology,Shanghai First people’s hospital,Shanghai Jiao Tong University,Shanghai 200080,China

Objective:To study the effect of U0126 on the expression of Bcl-2/Bax in neurons after hypoxic injury in ***:Brains from 1 day postnatal S-D rats were taken for in vitro neuron culture.3 days later,the cultures were divided randomly into three groups:drugtreated, hypoxia and normal *** in drug-treat and hypoxia group were subjected

关键词： hypoxic injury Apoptosis Mitogen activated protein kinases(MAPKs)

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Down-regulation of Cav1.2 by its Regulating Protein Calpastatin in Myocardial hypoxic-Ischemic injury

Down-regulation of Cav1.2 by its Regulating Protein Calpasta...

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者：胡慧媛毛楠晏珊孙宇王健王莹孙雪菲赵金生郝丽英中国医科大学药学院药物毒理学教研室

Our recent study has revealed that calpastatin,an endogenous calpain inhibitor,could not only reprime activity of Cav1.2 Ca2+channel from run-down in cell-free patches but also directly bind to intracellular C-terminal region of Cav1.2 ***,the pathophysiological role of Cav1.2-channel-regulating function of calpastatin was largely *** this study,we investigated the changes in expression and function of Cav1.2 channels associated with calpastatin in both in vitro H9c2 hypoxia model and in vivo myocardial infarction（MI）model of *** found that both m RNA and protein levels of Cav1.2 and calpastatin decreased at the late stage of hypoxic-ischemic（H-I）injury,which could not be prevented by administration of calpain inhibitor MDL *** the same time,influx of Ca2+induced by KCl wasattenuated in H9c2 cells confronted to *** addition,colocalization of Cav1.2 and calpastatin on the cytoplasmic membrane was observed in sham-operated rats,but it was only detected in cytosol in rats encountered *** of calpastatin with si RNA in H9c2 cells resulted in both decreased Cav1.2 levels and depressed Cav1.2 channel *** together,these results indicate that dysregulation of Cav1.2 Ca2+channel by calpastatin was involved in myocardial H-I injury,which provide insights that proper regulation of Cav1.2 Ca2+channel by calpastatin was needed in maintaining the normal cardiac function.

关键词： L type calcium channel Calpastatin Heart hypoxic injury Regulation

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Gender difference in the neuroprotective effect of rat bone marrow mesenchymal cells against hypoxiainduced apoptosis of retinal ganglion cells

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Neural Regeneration Research 2016年第5期11卷 846-853页

作者： Jing Yuan Jian-xiong Yu Eye Center Renmin Hospital of Wuhan University Wuhan Hubei Province China Department of Gastrointestinal Surgery Renmin Hospital of Wuhan University Wuhan Hubei Province China

Bone marrow mesenchymal stem cells can reduce retinal ganglion cell death and effectively prevent vision loss. Previously, we found that during differentiation, female rhesus monkey bone marrow mesenchymal stem cells acquire a higher neurogenic potential compared with male rhesus monkey bone marrow mesenchymal stem cells. This suggests that female bone marrow mesenchymal stem cells have a stronger neuroprotective effect than male bone marrow mesenchymal stem cells. Here, we first isolated and cultured bone marrow mesenchymal stem cells from female and male rats by density gradient centrifugation. Retinal tissue from newborn rats was prepared by enzymatic digestion to obtain primary retinal ganglion cells. Using the transwell system, retinal ganglion cells were co-cultured with bone marrow mesenchymal stem cells under hypoxia. Cell apoptosis was detected by flow cytometry and caspase-3 activity assay. We found a marked increase in apoptotic rate and caspase-3 activity of retinal ganglion cells after 24 hours of hypoxia compared with normoxia. Moreover, apoptotic rate and caspase-3 activity of retinal ganglion cells significantly decreased with both female and male bone marrow mesenchymal stem cell co-culture under hypoxia compared with culture alone, with more significant effects from female bone marrow mesenchymal stem cells. Our results indicate that bone marrow mesenchymal stem cells exert a neuroprotective effect against hypoxia-induced apoptosis of retinal ganglion cells, and also that female cells have greater neuroprotective ability compared with male cells.

关键词： nerve regeneration optic nerve injury bone marrow mesenchymal stem cells retinal ganglion cells neuroprotection hypoxic injury gender difference transwell system co-culture cell apoptosis flow cytometry caspase-3 neural regeneration

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The expression of SIRT3 signaling in hypoxia-induced endothelial injury

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South China Journal of Cardiology 2020年第4期21卷 277-284页

作者： CHEN Chun-juan LIN Mei-ling WANG Wei YU Wei Department of Cardiology Second Affiliated Hospital of Shantou University Medical CollegeShantou 515041China Department of Cardiology First Affiliated Hospital of Shantou University Medical CollegeShantou 515041China Department of Internal Medicine Xiang'an Hospital of Xiamen UniversityXiamen 361102China

Background Oxidative injury to the endothelial cells plays an important role in development of *** of the mechanisms of oxidative endothelial injury is of great *** previous report has demonstrated that Sirtuin 3(SIRT3)protect cardiomyocytes from oxidative stress-mediated cell death via activating the nuclear factor kappa-B(NF-κB)signaling ***,the role and exact mechanisms of SIRT3 signaling in endothelial hypoxia injury are largely *** present study aimed to investigate the expression of SIRT3,hypoxia-inducible factor 1α(HIF-1α),and NF-κB/TNF-α(tumor necrosis factor-α)in human umbilical vein endothelial cells(HUVECs)treated by *** Hypoxia model was established by anoxic tank and randomly divided into 3 groups:control group,1 h hypoxia group,and 3 h hypoxia group.3-(4,5-dimetrylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)detected the cell viability under hypoxia condition,and the intracellular reactive oxygen species(ROS)generation was determined by 2′,7′-Dichlorodihydrofluorescein diacetate(DCFH-DA).The expression of m RNA and protein of the SIRT3 signaling were detected by real-time quantitative polymerase chain reaction(q PCR)and western blot analysis,*** Hypoxia treatment time-dependently decreased the cell viability,especially in the first *** production significantly increased in the first hour of hypoxia compared with those in the second and the third *** stimuli significantly elevated SIRT3 m RNA and protein ***,real-time q PCR results showed that elevated SIRT3 significantly increased the m RNA expression of HIF-1αand NF-κB/TNF-αin 1 h hypoxia *** blot results also showed that elevated SIRT3 significantly increased the protein expression of NF-κB in the 1 h hypoxia *** The present study indicated that hypoxic stimuli promoted the expression of SIRT3,HIF-1α,and NF-κB/TNF-α,and suggested that SIRT3 signaling path

关键词： hypoxic injury human endothelial cells signaling pathway SIRT3

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