论文部分内容阅读
目的观察尾加压素Ⅱ(UⅡ)对心肌细胞凋亡的影响并探讨其作用机制。方法来自大鼠胚胎心脏细胞系的H9c2心肌细胞作为心脏细胞的体外实验模型。将细胞分为4组:对照组、10~(-9)mol·L~(-1)UⅡ处理组、10~(-8)mol·L~(-1)UⅡ处理组、10~(-7)mol·L~(-1)UⅡ处理组。利用ELISA方法检测各组细胞半胱氨酸蛋白酶3(caspase-3)的表达量,通过AnnexinV/PI双染法及流式细胞仪检测细胞凋亡率。结果与对照组相比,UⅡ处理后细胞内caspase-3的表达量降低(P<0.05),呈剂量依赖性;细胞凋亡率也呈剂量依赖性降低。结论 UⅡ可能通过下调caspase-3的表达而抑制H9c2心肌细胞的凋亡。
Objective To investigate the effect of urotensin Ⅱ on cardiomyocyte apoptosis and its mechanism. Methods H9c2 cardiomyocytes from rat embryonic heart cell lines were used as in vitro experimental models of cardiac cells. The cells were divided into 4 groups: control group, 10 -9 mol·L -1 UⅡ treatment group, 10 -8 mol·L -1 UⅡ treatment group, 7) mol·L -1 UⅡ treatment group. The expression of caspase-3 in each group was detected by ELISA. The apoptosis rate was detected by Annexin V / PI double staining and flow cytometry. Results Compared with the control group, the expression of caspase-3 in UⅡ treated group was decreased (P <0.05) in a dose-dependent manner and the apoptosis rate was also decreased in a dose-dependent manner. Conclusion UⅡ may inhibit the apoptosis of H9c2 cardiomyocytes by down-regulating the expression of caspase-3.