NaHS抑制创伤出血性休克导致的大鼠心肌组织的凋亡

目的:创伤导致的失血性休克是临床上常见的导致死亡的原因之一,传统的快速扩容措施会导致缺血-再灌注损伤,诱发炎症反应和组织细胞的凋亡坏死;新型气体信号分子硫化氢(H2S)具有抗炎、促进心血管增生等多种生理保护功能,在此实验中我们探索了新型气体信号分子硫化氢(H2S)对出血性休克大鼠心肌的保护作用。方法:复制雄性SD大鼠出血性休克模型:复制大鼠腹中正切口造成创伤模型,然后经右侧股动脉插管放血,造成失血性休克,右侧股静脉建立液体通道准备复苏,给药组大鼠经腹腔给予NaHS(28μmol/kg),经左侧股动脉插管至左心室监测大鼠血流动力学的影响;取大鼠复苏后2 h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凋亡相关因子Bcl-2、Bax、与Caspase-8的表达变化。结果:外源性H2S对创伤性休克大鼠的血流动力学指标有不同程度的改善,保护了创伤休克导致的心肌细胞的损伤,并上调了大鼠心肌组织中抗凋亡蛋白Bcl-2的表达,下调了促凋亡蛋白Bax及Caspase-8的表达。结论:外源性硫化氢可能通过抑制凋亡途径来保护创伤性休克导致大鼠的心肌组织的损伤,从而起到保护作用。

Exogenous H2S Protects Cardiac Tissue Through Inhibiting Apoptosis in a Traumatic-hemorrhagic Shock Rat Model

Objective： Trauma induced hemorrhagic shock is a common death reason clinically. Traditional rapid fluid infusion method will result in ischemia-reperfusion injury, inflammation response, and apoptosis even necrosis in cells or tissues. The new gaseous signaling molecule H2S possesses kinds of physiological protective funciotns such as anti-infammation and pro-angiogenesis. In the present study, we explored the protective effects of H2S on a mimetic traumatic-hemorrhagic shock rat model. Methods： Duplicate male SD rats traumatic-hemorrhagic shock models, hemodynamic data was recorded by inserting a PE-50 catheter to left femoral artery of the rats which were treated with NariS （28 μmol/kg） in advance. Two hours after injection NariS, the rats＇ vein blood was obtained. Serum CK and LDH levels were analyzed and Bcl-2, Bax and Caspase-8 in rat cardiac tissue were detected by Western-blot assays. Results： Exogenous H2S improved rats＇ hemodynamic function, protected rats＇ cardiac tissue from traumatic-hemorrhagic shock, up-regnlated ex-pression of Bcl-2 and down-regulated expression of the pro-apoptosis factors Bax and Caspase-8 in rats＇ cardiac tissue. Conclusion： Ex- ogenous H2S may exert cardio-protective effects through inhibiting apoptosis pathway.