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目的通过大鼠心肌缺血再灌注模型研究解酒药对缺血再灌注(IR)损伤的保护作用。方法雄性SD大鼠分为IR+生理盐水对照组、IR+解酒药组、IR+解酒药+cyanamide(乙醛脱氢酶2抑制剂,氨基氰,CH2N2)组。伊文思蓝和TTC染色评估心肌梗死面积,TUNEL法测定缺血再灌注区域心肌细胞凋亡情况,Western blot测定分析内质网应激相关蛋白Grp78和Chop含量变化以及凋亡相关蛋白Caspase12含量变化。结果解酒药减轻心肌梗死面积,而cyanamide的加入部分抵消了解酒药对心肌缺血再灌注的保护作用[IR+生理盐水对照组:(57.72±6.52)%;IR+解酒药组:(35.59±5.77)%;IR+解酒药+cyanamide组:(46.83±5.96)%;IR+生理盐水对照组vs.IR+解酒药组,P<0.01;IR+生理盐水对照组vs.IR+解酒药+cyanamide组,P<0.01;IR+解酒药组vs.IR+解酒药+cyanamide组,P<0.01]。Grp78、Chop、Caspase12蛋白水平于IR+生理盐水对照组、IR+解酒药组、IR+解酒药+cyanamide组中均无统计学差异(P>0.05)。结论在心肌缺血再灌注损伤早期,解酒药对心肌缺血再灌注损伤具有保护作用,且抑制ALDH2后此作用消失,但其机制可能不是通过调控ALDH2参与的内质网应激而实现的。
Objective To study the protective effect of hangover on ischemia-reperfusion (IR) injury in rat model of myocardial ischemia-reperfusion. Methods Male Sprague-Dawley rats were divided into three groups: IR + saline control group, IR + anti-alcoholic drug group and IR + anti-alcohol drug + cyanamide (aldehyde dehydrogenase 2 inhibitor, cyanamide, CH2N2) group. Evans blue and TTC staining were used to evaluate the area of myocardial infarction. TUNEL method was used to detect the apoptosis of myocardial cells in ischemia-reperfusion area. Western blot was used to analyze the content of Grp78 and Chop in endoplasmic reticulum and the content of Caspase12. Results anti-alcohol drug to reduce myocardial infarction area, while the addition of cyanamide partially offset the protective effect of alcohol on myocardial ischemia-reperfusion [IR + saline control group: (57.72 ± 6.52)%; IR + hangover group: (35.59 ± (46.83 ± 5.96)%; IR + saline control group vs.IR + hangover group, P <0.01; IR + saline control group vs.IR + hangover agent + cyanamide group , P <0.01; IR + hangover group vs.IR + hangover + cyanamide group, P <0.01]. Grp78, Chop, Caspase12 protein levels in the IR + saline control group, IR + anti-alcoholic drug group, IR + anti-alcoholic drugs + cyanamide group were no significant difference (P> 0.05). Conclusion In the early stage of myocardial ischemia-reperfusion injury, anti-alcohol drugs have a protective effect on myocardial ischemia-reperfusion injury, and the effect disappeared after inhibiting ALDH2, but the mechanism may not be through the regulation of ERDH2 endoplasmic reticulum stress .