氯化钴诱导HIF-1α增高拮抗过氧化氢引起的人骨肉瘤MG-63细胞凋亡  

Antagonism effects of cobalt chloride with increasing HIF-1α on apoptosis of human osteosarcoma MG-63 cells induced by H_2O_2

作　　者：黄海涛[1] 梁单[2] 刘司琪[1] 刘胜权[1] 朱树福[1] 金昱[3] 

机构地区：[1]中国人民解放军95988部队后勤部门诊部 [2]中国人民解放军95935部队 [3]延边大学医学院人体解剖学教研部

出　　处：《延边大学医学学报》2013年第1期6-10,共5页Journal of Medical Science Yanbian University

摘　　要：[目的]验证氯化钴抑制过氧化氢诱导的人骨肉瘤MG-63细胞的凋亡作用并探讨其可能的分子机制.[方法]将人骨肉瘤MG-63细胞分为正常对照组、过氧化氢组、过氧化氢+氯化钴预处理组、过氧化氢+氯化钴+YC-1组.应用MTT法测定细胞存活率;流式细胞术测定细胞凋亡;免疫荧光染色、蛋白印迹法检测HIF-1α表达.[结果]与过氧化氢组比较,氯化钴预处理组细胞存活率明显增加(P<0.05);凋亡细胞比率降低.缺氧可激活HIF-1α的表达并诱导其转位,100μmol/L氯化钴可明显增加HIF-1α蛋白的表达(P<0.01).[结论]氯化钴可抑制过氧化氢诱导的人骨肉瘤MG-63细胞的凋亡,其分子机制可能与激活HIF-1α的表达有关.OBJECTIVE To study the antagonism effects and its possible molecular mechanism of cobalt chloride（CoC12） on apoptosis of human osteosarcoma MG-63 cells induced by H202. METHODS MG-63 cells were divided into 4 groups of control group, H202 group, H202 ＋ COC12 and H202 ＋ COC12 ＋ YC-1 group, and the survival rate of MG-63 cells was measured by MTT, the apoptosis of MG-63 cells was detected by flow cytometry, and the expression of HIF-la was determined by immunofluorescence and Western Blot. RESULTS As compared with H202 group, the survival rate of MG-63 cells increased significantly in pretreatment group with COC12 （P 〈0.05） and apoptosis rate of MG-63 cells decreased. Hypoxia could activate the expression of HIF-la and induced its translocation. 100 μmol/L of COC12 were significantly up-regulated the expression of HIF-la protein in MG-63 cells. CONCLUSION The COC12 inhibits the apoptosis of human osteosarcoma MG-63 cells induced by H202, and its molecular mechanism is related to activating the expression of HIF-la.

关 键 词：细胞凋亡 氯化钴 缺氧诱导因子1 Α亚基 过氧化氢 骨肉瘤 

分 类 号：R738[医药卫生—肿瘤]