{"title":"褪黑素对脑损伤神经元的保护作用与bcl-2蛋白过表达有关。","authors":"X Ling, L M Zhang, S D Lu, X J Li, F Y Sun","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>To study the protective effect of melatonin against neuronal injury and the possible roles of alteration in the expression of bcl-2 and bax following brain ischemia.</p><p><strong>Methods: </strong>Brain ischemia was induced by left middle cerebral artery occlusion (MCAO) for 60 min in rats. Brain damage was evaluated by the infarct area and the neuronal cell counting. The expression of bcl-2 and bax was analyzed by immunohistochemical method.</p><p><strong>Results: </strong>Melatonin decreased the infarct area and prevented the neuronal death after 24-h reperfusion following 1-h MCAO. Melatonin given before the ischemia enhanced the expression of bcl-2 in the penumbra area and had no significant effect on the expression of bax.</p><p><strong>Conclusion: </strong>Melatonin effectively attenuated ischemic brain injury and increased the expression of neuronal bcl-2 in the ischemic brain, indicating that the protective effect of melatonin was associated with up-regulation of bcl-2 in ischemia-induced neuronal death.</p>","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1999-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Protective effect of melatonin on injuried cerebral neurons is associated with bcl-2 protein over-expression.\",\"authors\":\"X Ling, L M Zhang, S D Lu, X J Li, F Y Sun\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Aim: </strong>To study the protective effect of melatonin against neuronal injury and the possible roles of alteration in the expression of bcl-2 and bax following brain ischemia.</p><p><strong>Methods: </strong>Brain ischemia was induced by left middle cerebral artery occlusion (MCAO) for 60 min in rats. Brain damage was evaluated by the infarct area and the neuronal cell counting. The expression of bcl-2 and bax was analyzed by immunohistochemical method.</p><p><strong>Results: </strong>Melatonin decreased the infarct area and prevented the neuronal death after 24-h reperfusion following 1-h MCAO. Melatonin given before the ischemia enhanced the expression of bcl-2 in the penumbra area and had no significant effect on the expression of bax.</p><p><strong>Conclusion: </strong>Melatonin effectively attenuated ischemic brain injury and increased the expression of neuronal bcl-2 in the ischemic brain, indicating that the protective effect of melatonin was associated with up-regulation of bcl-2 in ischemia-induced neuronal death.</p>\",\"PeriodicalId\":24002,\"journal\":{\"name\":\"Zhongguo yao li xue bao = Acta pharmacologica Sinica\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1999-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Zhongguo yao li xue bao = Acta pharmacologica Sinica\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Protective effect of melatonin on injuried cerebral neurons is associated with bcl-2 protein over-expression.
Aim: To study the protective effect of melatonin against neuronal injury and the possible roles of alteration in the expression of bcl-2 and bax following brain ischemia.
Methods: Brain ischemia was induced by left middle cerebral artery occlusion (MCAO) for 60 min in rats. Brain damage was evaluated by the infarct area and the neuronal cell counting. The expression of bcl-2 and bax was analyzed by immunohistochemical method.
Results: Melatonin decreased the infarct area and prevented the neuronal death after 24-h reperfusion following 1-h MCAO. Melatonin given before the ischemia enhanced the expression of bcl-2 in the penumbra area and had no significant effect on the expression of bax.
Conclusion: Melatonin effectively attenuated ischemic brain injury and increased the expression of neuronal bcl-2 in the ischemic brain, indicating that the protective effect of melatonin was associated with up-regulation of bcl-2 in ischemia-induced neuronal death.