缺氧预适应减轻乳鼠心肌细胞缺氧性损伤

目的 探讨缺氧预适应对缺氧—复氧损伤的乳鼠心肌细胞的保护作用。方法 第2代心肌细胞随机分为对照组(C组)、缺氧—复氧组(A—R组)和缺氧预适应组(AP组)，每组均缺氧2h，复氧48h。取复氧心肌细胞，用电镜观察细胞超微结构变化、MTT法测定细胞生存情况、流式细胞仪测定细胞凋亡率、免疫组化染色检测HSP10表达。结果 (1)AP组细胞超微结构改变不明显，未见凋亡细胞；A—R组可见凋亡细胞。(2)各时点AP组的细胞存活数显著低于C组(P＜0．05)；显著高于A—R组(P＜0．01)；且随复氧时间延长有增加趋势。(3)各时点AP组的细胞凋亡率显著高于C组；显著低于A—R组(P＜0．01)；随复氧时间延长，AP组细胞凋亡率有下降趋势，A—R组则逐渐升高。(4)各时点AP组HSP70表达显著高于其余各组(P＜0．01)；AP组HSP70表达从1h处开始增加，24h处表达最强(P＜0．01)。结论 (1)A-R对心肌细胞确有损伤作用。(2)AP对A—R损伤能产生早期和延迟保护作用。(3)HSP70可能参与了AP的延迟保护作用。

Anoxia-induced preconditioning reduces anoxia injury of cardiomyocytes in neonatalrat

Objective To investigate the role of anoxia preconditioning in protecting neonatal rat cardiomyocytes from anoxia reoxygenation injury.Methods The second generations of primary cultured cardiomyocytes were randomly divided into 3 groups:control(group C),anoxia/reoxygenation(group A/R) and anoxia preconditioning(group AP).The cardiomyocytes were exposed to a 2h anoxia,followed by a 48h reoxygenation for each group.The ultrastructure changes of cardiomyocytes after 1h reoxygenation were detected,and the cell survival ability,cell apoptosis percentage,and HSP 70 expression at 0,1,12,24,36 and 48h after reoxygenation were measured respectively.Results (1)Little change of the cellular ultrastructure occurred in group AP,and apoptosis cells were not found.However,apoptosis cells were found in group A/R.(2)At each time point of reoxygenation,the survival in group AP was higher than that in group A/R,lower than that in group C( P< 0 05).The survival of group AP increased with the prolongation of reoxygenation time( P< 0 01).(3)The apoptosis percentage of cells in group AP was significantly higher than that in group C,and lower than that in group A/R( P< 0 01).With the prolongation of reoxygenation,the apoptosis percentage had a descending terdancy in group AP,and an ascending terdancy in group A/R.(4)At each time point of reoxygenation,the expression of HSP 70 in group AP was significantly higher than that in other groups( P< 0 01).With the prolongation of reoxygenation,the HSP70 expression in group AP increased starting from 1h after reoxygenation,and reaching to the peak at the 24h reoxygenation( P< 0 01).Conclusion (1)Anoxia reoxygenation injuried the cardiomyocytes.(2)Anoxia preconditioning can produce a protection effect on the myocardium during early and delayed phase of A/R injury.(3)HSP 70 may be involved in the delayed protection phase of anoxia preconditioning.