CAJ | 학술논문

观察内皮细胞在高糖环境及经肿瘤坏死因子α(TNF-α)诱导后的细胞凋亡情况,并加入自由基清除剂MCI-186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MCI-186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TNF-α诱导的调亡.MCI-186可抑制高糖诱导的细胞凋亡.但无法干预高糖环境中TNF-a诱导的凋亡.
관찰내피세포재고당배경급경종류배사인자α(TNF-α)유도후적세포조망정황,병가입자유기청제제MCI-186여이간우.검측세포DNA렬해편단급조망신호단백(caspase)적표체량,이기탐토MCI-186대고당배경중혈관내피세포조망적간예작용급조망궤제.발현고당배경가증가내피세포조망솔,병상조TNF-α유도적조망.MCI-186가억제고당유도적세포조망.단무법간예고당배경중TNF-a유도적조망.
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.