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作 者:董叫云[1] 高見佳宏 青春[1] 田中秀治[2] 山口亮 郭静苹[2] 尾乡贤 陆树良[1]
机构地区:[1]上海第二医科大学附属瑞金医院,上海市烧伤研究所,200025 [2]日本杏林大学医学院形成外科及热伤中心
出 处:《中华糖尿病杂志(1006-6187)》2005年第3期234-235,共2页
基 金:国家重点研究发展规划项目资助(G1999054205)
摘 要:观察内皮细胞在高糖环境及经肿瘤坏死因子α(TNFα)诱导后的细胞凋亡情况,并加入自由基清除剂MCI186予以干扰。检测细胞DNA裂解片段及凋亡信号蛋白(caspase)的表达量,以期探讨MCI186对高糖环境中血管内皮细胞凋亡的干预作用及凋亡机制。发现高糖环境可增加内皮细胞凋亡率,并上调TNFα诱导的调亡。MCI186可抑制高糖诱导的细胞凋亡。但无法干预高糖环境中TNFa诱导的凋亡。In the present study, the role of a free radical scavenger (MCI-186) in preventing endothelial cell apoptosis induced by high glucose condition was studied. HDMEC were incubated with high glucose medium, with or without MCI-186. After 7 days of incubation, cell apoptosis with or without TNF-alpha was detected through DNA fragment and caspase assay. High glucose condition could enhance cell apoptosis and up-regulate TNF-alpha induced cell apoptosis. Based on the data of caspase-8 and caspase-3, TNF-alpha induced EC apoptosis might occur through mitochondria death pathway dominantly on high glucose condition. MCI-186 might suppress high glucose-induced cell apoptosis, however, it did not alter TNF-alpha induced apoptosis. These results suggest that MCI-186 may be useful in preventing endothelial cell damages by high glucose condition.
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