Bo Zhang, Xiao-qin Wang, Hanying Chen, Qiusheng Zheng, Xin Li
{"title":"GSH耗竭在白藜芦醇诱导HeLa细胞凋亡中的作用","authors":"Bo Zhang, Xiao-qin Wang, Hanying Chen, Qiusheng Zheng, Xin Li","doi":"10.1109/ISB.2011.6033113","DOIUrl":null,"url":null,"abstract":"The dual role of Resveratrol (Rsv) in cell apoptosis was recently reported by its anti/pro-oxidant activities. The involvement of ROS and GSH was thus investigated in Rsv-induced HeLa cell apoptosis. Rsv, higher than 10µM, elevated the intracellular ROS but reduced O2•− and GSH levels. ROS scavengers (Tempol, catalase) could not inhibit the apoptosis. Treatment with GSH modulators DTT or BSO were resulted up-regulation or down-regualtion GSH levels, but both enhanced Rsv-induced HeLa cell apoptosis. However, BSO could not prevent the DTT+Rsv treated HeLa cells from apoptosis. Further, Rsv-induced HeLa cell apoptosis was accompanied by activation of caspase 3 but not caspase 9, neither did the loss of mitochondrial membrane potential. Conclusively, the changes of ROS by Rsv were not tightly correlated with apoptosis in HeLa cells. However, intracellular GSH levels are partially related to Rsv-induced HeLa cell apoptosis via a mitochondrial independent manner.","PeriodicalId":355056,"journal":{"name":"2011 IEEE International Conference on Systems Biology (ISB)","volume":"19 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2011-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"The role of GSH depletion in Resveratrol induced HeLa cell apoptosis\",\"authors\":\"Bo Zhang, Xiao-qin Wang, Hanying Chen, Qiusheng Zheng, Xin Li\",\"doi\":\"10.1109/ISB.2011.6033113\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The dual role of Resveratrol (Rsv) in cell apoptosis was recently reported by its anti/pro-oxidant activities. The involvement of ROS and GSH was thus investigated in Rsv-induced HeLa cell apoptosis. Rsv, higher than 10µM, elevated the intracellular ROS but reduced O2•− and GSH levels. ROS scavengers (Tempol, catalase) could not inhibit the apoptosis. Treatment with GSH modulators DTT or BSO were resulted up-regulation or down-regualtion GSH levels, but both enhanced Rsv-induced HeLa cell apoptosis. However, BSO could not prevent the DTT+Rsv treated HeLa cells from apoptosis. Further, Rsv-induced HeLa cell apoptosis was accompanied by activation of caspase 3 but not caspase 9, neither did the loss of mitochondrial membrane potential. Conclusively, the changes of ROS by Rsv were not tightly correlated with apoptosis in HeLa cells. However, intracellular GSH levels are partially related to Rsv-induced HeLa cell apoptosis via a mitochondrial independent manner.\",\"PeriodicalId\":355056,\"journal\":{\"name\":\"2011 IEEE International Conference on Systems Biology (ISB)\",\"volume\":\"19 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2011-10-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"2011 IEEE International Conference on Systems Biology (ISB)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1109/ISB.2011.6033113\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"2011 IEEE International Conference on Systems Biology (ISB)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1109/ISB.2011.6033113","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The role of GSH depletion in Resveratrol induced HeLa cell apoptosis
The dual role of Resveratrol (Rsv) in cell apoptosis was recently reported by its anti/pro-oxidant activities. The involvement of ROS and GSH was thus investigated in Rsv-induced HeLa cell apoptosis. Rsv, higher than 10µM, elevated the intracellular ROS but reduced O2•− and GSH levels. ROS scavengers (Tempol, catalase) could not inhibit the apoptosis. Treatment with GSH modulators DTT or BSO were resulted up-regulation or down-regualtion GSH levels, but both enhanced Rsv-induced HeLa cell apoptosis. However, BSO could not prevent the DTT+Rsv treated HeLa cells from apoptosis. Further, Rsv-induced HeLa cell apoptosis was accompanied by activation of caspase 3 but not caspase 9, neither did the loss of mitochondrial membrane potential. Conclusively, the changes of ROS by Rsv were not tightly correlated with apoptosis in HeLa cells. However, intracellular GSH levels are partially related to Rsv-induced HeLa cell apoptosis via a mitochondrial independent manner.