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目的:研究缺血预适应对大鼠心肌缺血再灌注损伤的保护作用是否由toll样受体4(TLR4)/NF-κB途径所介导,以及是否与促进降钙素基因相关肽(CGRP)释放有关。方法:结扎Sprague-Dawley大鼠左冠状动脉前降支60 min,复灌3 h造成心肌缺血再灌注损伤。缺血预适应为结扎大鼠左冠状动脉前降支5 min,复灌5 min,共4个周期。RT-PCR分析心肌TLR4 mRNA表达。免疫组织化学法分析心肌TLR4和NF-κB蛋白表达。同时,测定心肌梗死面积、血浆CGRP浓度和血清肌酸激酶活性。结果:缺血预适应显著减少心肌梗死面积,降低肌酸激酶活性,增高血浆CGRP水平。心肌缺血再灌注可显著上调TLR4和NF-κB表达,缺血预适应可抑制其作用。结论:缺血预适应通过抑制TLR4/NF-κB信号通路保护大鼠心肌缺血再灌注损伤,其作用与促进CGRP释放有关。
AIM: To investigate whether the protective effect of ischemic preconditioning on myocardial ischemia-reperfusion injury in rats is mediated by the toll-like receptor 4 (TLR4) / NF-κB pathway and whether it is associated with the promotion of calcitonin gene-related peptide Released. Methods: Ligation of left anterior descending coronary artery of Sprague-Dawley rats for 60 min and reperfusion for 3 h resulted in myocardial ischemia-reperfusion injury. Ischemic preconditioning ligation of left anterior descending coronary artery 5 min, reperfusion 5 min, a total of 4 cycles. RT-PCR analysis of myocardial TLR4 mRNA expression. Immunohistochemical analysis of TLR4 and NF-κB protein expression in myocardium. At the same time, myocardial infarct size, plasma CGRP concentration and serum creatine kinase activity were determined. Results: Ischemic preconditioning significantly reduced myocardial infarct size, decreased creatine kinase activity and increased plasma CGRP levels. Myocardial ischemia-reperfusion can significantly up-regulate the expression of TLR4 and NF-κB, and ischemic preconditioning can inhibit its effect. CONCLUSION: Ischemia preconditioning protects rat against myocardial ischemia-reperfusion injury by inhibiting TLR4 / NF-|ÊB signaling pathway, which is related to the promotion of CGRP release.