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目的:探讨囊性纤维化跨膜传导调节因子(CFTR)氯通道在硫化氢(H2S)诱导的心肌保护及细胞增殖中的作用。方法:应用氯化钴(CoCl2)在大鼠H9c2心肌细胞建立化学性缺氧损伤心肌细胞实验模型;CCK-8试剂盒检测心肌细胞存活率;Hoechst 33342核染色法检测心肌细胞凋亡。结果:在400-2 000μmol/L浓度范围内,CoCl2呈剂量依赖性地抑制H9c2心肌细胞的存活率,600μmol/L CoCl2能诱导H9c2心肌细胞产生明显的凋亡;在100-800μmol/L浓度范围内,硫氢化钠(NaHS)呈剂量依赖性地促进H9c2心肌细胞增殖;NaHS能保护H9c2心肌细胞对抗CoCl2引起的细胞损伤作用,使细胞存活率升高,凋亡率降低;100μmol/L CFTR氯通道拮抗剂5-硝基-2-(3-苯丙胺)-苯甲酸(NPPB)能明显地阻断NaHS对CoCl2的细胞毒性的抑制作用,但不能阻断NaHS抗心肌细胞凋亡作用及促进心肌细胞增殖作用。结论:CFTR氯通道可能参与H2S的抗CoCl2引起的心肌细胞毒性作用。
Objective: To investigate the role of cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel in hydrogen sulfide (H2S) -induced myocardial protection and cell proliferation. Methods: Experimental hypoxia-injured cardiomyocytes were established by using cobalt chloride (CoCl2) in rat H9c2 cardiomyocytes. Cardiomyocyte survival rate was detected by CCK-8 kit. Cardiomyocyte apoptosis was detected by Hoechst 33342 nuclear staining. Results: In the concentration range of 400-2 000μmol / L, CoCl2 inhibited the survival rate of H9c2 cardiomyocytes in a dose-dependent manner. At the concentration of 100-800μmol / L, the apoptosis of H9c2 cells was induced by 600μmol / NaHS could promote H9c2 cardiomyocyte proliferation in a dose-dependent manner. NaHS could protect H9c2 cells against CoCl2-induced cell injury and increase cell viability and decrease apoptosis rate. Natrium chloride (100μmol / L) The channel antagonist 5-nitro-2- (3-amphetamine) -benzoic acid (NPPB) could obviously block the inhibitory effect of NaHS on the cytotoxicity of CoCl2, but could not block NaHS against cardiomyocyte apoptosis and promote myocardium Cell proliferation. Conclusion: CFTR chloride channels may be involved in the anti-CoCl2-induced cytotoxicity of H2S.