【摘要】 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。更多还原

【Abstract】 AIM: To explore the roles of cystic fibrosis transmembrane conductance regulator(CFTR) Cl-channels in hydrogen sulfide(H2S)-induced cardioprotection and cell proliferation in H9c2 cells.METHODS: Cobalt chloride(CoCl2) was used to set up the chemical hypoxia-induced injury model in H9c2 cells.Myocardial cell viability was detected by the CCK-8 assay kit.Apoptotic changes in H9c2 cells were observed by using Hoechst 33342 staining and photofluorography.RESULTS: At the concentrations from 400 to 2 000 μmol/L,CoCl2 dose-dependently inhibited cell viability in H9c2 cells.CoCl2 at concentration of 600 μmol/L significantly induced H9c2 cell apoptosis.Sodium hydrosulfide(NaHS) at concentrations from 100 to 400 μmol/L dose-dependently enhanced proliferation in H9c2 cells.NaHS protected H9c2 cells against CoCl2-induced injury,including an increase in cell viability and a decrease in percentage of apoptosis.5-nitro-2-(3-phenylpropylamino)-benzoic acid(NPPB,100 μmol/L),an inhibitor of CFTR Cl-channels alone did not damaged H9c2 cells,but considerably blocked the inhibitory effect of NaHS on CoCl2 cytotoxicity.However,NPPB did not antagonize the NaHS-induced antiapoptotic effect and cell proliferation in H9c2 cells.CONCLUSION: CFTR Cl-channels may be involved in the inhibitory effect of H2S on CoCl2-induced cytotoxicity in H9c2 cells.更多还原