Ru-juan Xin, Ting Zhao, Min Ni, Dong-Jie Li, F. Shen
{"title":"α - 7烟碱乙酰胆碱受体的激活可减轻氧-葡萄糖剥夺所致的大脑皮质神经元损伤","authors":"Ru-juan Xin, Ting Zhao, Min Ni, Dong-Jie Li, F. Shen","doi":"10.3724/SP.J.1008.2015.00472","DOIUrl":null,"url":null,"abstract":"Objective To investigate the effect of activating α7 nicotinic acetylcholine receptor(α7n AchR) on cerebral cortical neurons injury induced by oxygen-glucose deprivation(OGD) and the possible mechanism.Methods Cerebral cortical neurons cultured for 7 d were randomly divided into three groups: control group,OGD group(Cells experienced a 12 h oxygen-glucose deprivation) and OGD group treated with PNU-282987(Cells experienced a 12 h oxygen-glucose deprivation with PNU-282987 pretreatment for 24 h).Cell viability was determined by CCK-8 assay,lactate dehydrogenase(LDH) was examined to reflect cell injury,apoptosis and reactive oxygen species(ROS) production were analyzed by flow cytometry,and expression of hemeoxygenase-1(HO-1) and hypoxia inducible factor-1α(HIF-1α) were detected by Western blotting analysis.Results OGD resulted in cell death,LDH increase,and cell apoptosis.Compared with the OGD group,PNU-282987 pretreated group had significantly increased cell survival(P 0.05),significantly decreased LDH level and ROS production(P 0.05),and significantly inhibited cell apoptosis(P 0.05).Meanwhile,HO-1 protein expression was significantly increased and HIF-1α protein expression was significantly reduced in PNU-282987 pretreated group compared with the OGD group(P 0.05).Conclusion Activation of α7n AchR can protect cerebral cortical neurons against OGD-induced injury,which may be related to the anti-oxidative stress.","PeriodicalId":6893,"journal":{"name":"海军军医大学学报","volume":"36 1","pages":"472"},"PeriodicalIF":0.0000,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Activation of α7 nicotinic acetylcholine receptor alleviates cerebral cortical neuron injury induced by oxygen-glucose deprivation\",\"authors\":\"Ru-juan Xin, Ting Zhao, Min Ni, Dong-Jie Li, F. Shen\",\"doi\":\"10.3724/SP.J.1008.2015.00472\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective To investigate the effect of activating α7 nicotinic acetylcholine receptor(α7n AchR) on cerebral cortical neurons injury induced by oxygen-glucose deprivation(OGD) and the possible mechanism.Methods Cerebral cortical neurons cultured for 7 d were randomly divided into three groups: control group,OGD group(Cells experienced a 12 h oxygen-glucose deprivation) and OGD group treated with PNU-282987(Cells experienced a 12 h oxygen-glucose deprivation with PNU-282987 pretreatment for 24 h).Cell viability was determined by CCK-8 assay,lactate dehydrogenase(LDH) was examined to reflect cell injury,apoptosis and reactive oxygen species(ROS) production were analyzed by flow cytometry,and expression of hemeoxygenase-1(HO-1) and hypoxia inducible factor-1α(HIF-1α) were detected by Western blotting analysis.Results OGD resulted in cell death,LDH increase,and cell apoptosis.Compared with the OGD group,PNU-282987 pretreated group had significantly increased cell survival(P 0.05),significantly decreased LDH level and ROS production(P 0.05),and significantly inhibited cell apoptosis(P 0.05).Meanwhile,HO-1 protein expression was significantly increased and HIF-1α protein expression was significantly reduced in PNU-282987 pretreated group compared with the OGD group(P 0.05).Conclusion Activation of α7n AchR can protect cerebral cortical neurons against OGD-induced injury,which may be related to the anti-oxidative stress.\",\"PeriodicalId\":6893,\"journal\":{\"name\":\"海军军医大学学报\",\"volume\":\"36 1\",\"pages\":\"472\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2015-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"海军军医大学学报\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3724/SP.J.1008.2015.00472\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"海军军医大学学报","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3724/SP.J.1008.2015.00472","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
Activation of α7 nicotinic acetylcholine receptor alleviates cerebral cortical neuron injury induced by oxygen-glucose deprivation
Objective To investigate the effect of activating α7 nicotinic acetylcholine receptor(α7n AchR) on cerebral cortical neurons injury induced by oxygen-glucose deprivation(OGD) and the possible mechanism.Methods Cerebral cortical neurons cultured for 7 d were randomly divided into three groups: control group,OGD group(Cells experienced a 12 h oxygen-glucose deprivation) and OGD group treated with PNU-282987(Cells experienced a 12 h oxygen-glucose deprivation with PNU-282987 pretreatment for 24 h).Cell viability was determined by CCK-8 assay,lactate dehydrogenase(LDH) was examined to reflect cell injury,apoptosis and reactive oxygen species(ROS) production were analyzed by flow cytometry,and expression of hemeoxygenase-1(HO-1) and hypoxia inducible factor-1α(HIF-1α) were detected by Western blotting analysis.Results OGD resulted in cell death,LDH increase,and cell apoptosis.Compared with the OGD group,PNU-282987 pretreated group had significantly increased cell survival(P 0.05),significantly decreased LDH level and ROS production(P 0.05),and significantly inhibited cell apoptosis(P 0.05).Meanwhile,HO-1 protein expression was significantly increased and HIF-1α protein expression was significantly reduced in PNU-282987 pretreated group compared with the OGD group(P 0.05).Conclusion Activation of α7n AchR can protect cerebral cortical neurons against OGD-induced injury,which may be related to the anti-oxidative stress.
期刊介绍:
Founded in 1980, Academic Journal of Second Military Medical University(AJSMMU) is sponsored by Second Military Medical University, a well-known medical university in China. AJSMMU is a peer-reviewed biomedical journal,published in Chinese with English abstracts.The journal aims to showcase outstanding research articles from all areas of biology and medicine,including basic medicine(such as biochemistry, microbiology, molecular biology, genetics, etc.),clinical medicine,public health and epidemiology, military medicine,pharmacology and Traditional Chinese Medicine),to publish significant case report, and to provide both perspectives on personal experiences in medicine and reviews of the current state of biology and medicine.