外源性H_2S通过抑制凋亡途径保护创伤出血性休克大鼠心肌组织

Exogenous H_2S Protects Cardiac Tissue Through Inhibiting Apoptosis in a Traumatic-hemorrhagic Shock Rat Model

目的探索新型气体信号分子硫化氢(H2S)对创伤出血性休克大鼠心肌的保护作用。方法复制雄性SD大鼠创伤出血性休克模型,经左侧股动脉插管监测硫化氢的外源性供体NaHS干预(28μmol/kg)对创伤出血性休克大鼠血流动力学的影响;在注射NaHS2h后取静脉血,测量血清肌酸激酶(CK)及乳酸脱氢酶(LDH)水平,比较各组心肌酶改变;以蛋白印记法观察大鼠心肌组织survivin(生存素)以及促凋亡因子caspase-3与Bax的表达变化。结果外源性H2S对创伤出血性休克大鼠的血流动力学指标有不同程度的改善,上调了survivin的蛋白表达,下调了凋亡促进因子caspase-3及Bax的表达。结论外源性H2S可能通过影响凋亡的途径来保护创伤出血性休克大鼠的心肌组织,从而起到保护作用。

Objective To explore the cardio - protective effects of the third gaseous signaling molecule, H2 S, on a traumatic - hem- orrhagic shock rat model. Methods Male SD rats traumatic -hemorrhagic shock models were duplicated. Hemodynamic data was recor- ded by inserting a PE -50 catheter to left femoral artery of the rats which were treated with NariS （281xmol/kg） previously. Then the rats＇ vein blood 2 hours after injection of NariS were obtained. Serum CK and LDH levels were analyzed and Survivin,easpase - 3 and Bax in rat cardiac tissue were detected by western - blotting assay. Results Exogenous H2S improved rats＇ hemodynamic function, up - regula- ted expression of survivin and down - regulated expression of the pro - apoptosis factors caspase - 3 and Bax. Conclusion Exogenous H2S may have cardioprotective effects through modulating apoptosis pathway.