摘要
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。
AIM To investigate the effect of urotensin Ⅱ （U Ⅱ ） on apoptosis of H9c2 cells and its action mecha- nism. METHODS H9c2 cells derived from rat cardiac cell line were cultured as heart cell model in vitro. H9c2 cells were divided into control group, 10- 9 mol· L- 1 U Ⅱ group, 10- s mol· L- I U Ⅱ group and 10- 7 mol· L- 1 U Ⅱ group. Ex- pressions of caspase-3 were detected by enzyme-linked immunosorbent assay（ELISA）. After stained with Annexin V/PI , the apoptosis of H9c2 cells was assessed by flow cytometry. RESULTS Comparing with control group, the expression level of caspase-3 in H9c2 ceils and the apoptosis level of H9c2 ceils were significantly lower （P 〈 0.05） after treated with U Ⅱ , which were dose-dependent. CONCLUSION U Ⅱ can suppress apoptosis of H9c2 cells by down-regulating the expression of caspase-3.
出处
《中国临床药学杂志》
CAS
2016年第1期1-4,共4页
Chinese Journal of Clinical Pharmacy
基金
山西省自然科学基金(编号2012011036-1)
