缺氧预处理对 L02肝细胞Bcl-2、Bax、Fas及FasL表达的影响

目的:研究缺氧预处理对正常肝细胞株L02缺血再灌注损伤的抗凋亡机制.方法:将体外培养的L02细胞分为3组:正常对照组(A组)、缺氧复氧损伤组(B组)、缺氧预处理组(C组).各组细胞缺氧复氧处理1、6、1 2、18、24 h后,使用流式细胞术检测细胞凋亡率,各组细胞分别缺氧复氧、缺氧预处理后12 h检测细胞Bcl 2、Bax、Fas及FasL蛋白表达,同时对细胞结构进行电镜观察.结果:C组和B组比较,细胞凋亡率明显降低(P＜0.05),细胞Bcl-2蛋白表达明显升高(P＜0.05),Bax、Fas及FasL蛋白表达量显著降低(P＜0.05),透射电镜观察到缺氧预处理组细胞结构基本正常.结论:缺氧预处理明显减轻了缺氧复氧所导致的L02肝细胞损伤,降低了细胞凋亡率,缺氧预处理保护机制和Bcl-2、Bax、Fas及FasL蛋白表达有关.

Impact of hypoxia-precondition on expression of Bcl-2, Bax, Fas and FasL in liver cell line L02 during ischemia-reperfusion injury

Objective:To elucidate the protective mechanism of hypoxia-precondition on liver cell line L02apoptosis in-duced by hypoxia-reoxygenation injury in vitro.Methods:Cultured L02cells were divided into3groups:control(Group A), hypoxia-reoxygenation(Group B)and hypoxia-precondition(Group C).The apoptotic rate was detected with flow cytometric analysis when hypoxia-reperfusion was performed in all the3groups on1,6,12,18and24h.The expression of apoptosis-re-lated proteins(Bcl-2,Bax,Fas and FasL)was detected12h after hypoxia-reoxygenation and the cell structure was observed by transmission electron microscope.Results:Compared with Group B,the apoptotic rate in Group C decreased significantly (P< 0.05) and the expression of Bcl-2increased significantly(P<0.05),while the expression of Bax,Fas and FasL decreased(P <0.05).Conclusion:Hypoxia-precondition can inhibit the apoptosis induced by hypoxia-reoxygenation in L02cells,and the protective effect is related to the expression of Bcl-2,Bax,Fas and FasL.