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目的:评估糖原合酶激酶-3β(GSK-3β)抑制剂TDZD-8减轻大鼠急性心肌缺血/再灌注损伤(MIRI)的作用,并探讨此作用是否与其下调NF-κB、抑制炎症有关。方法:取健康雄性SD大鼠60只,随机分为缺血/再灌注(I/R)组、I/R+TDZD组、I/R+载体(Vehicle,V)组及假手术(Sham)组。大鼠局部心肌缺血30 min,再灌注3 h。用TTC染色计算心肌梗死面积,HE染色及ELISA法评估心肌组织中中性粒细胞浸润及炎性因子(TNF-α和IL-6)的变化;用Western blot测定心肌组织中NF-κB、GSK-3β磷酸化的水平。结果:TDZD-8能明显降低心肌梗死的面积和心肌组织中性粒细胞浸润、抑制NF-κB激活以及心肌源性TNF-α和IL-6的浓度(P<0.01)。结论:GSK-3β抑制剂TDZD-8能够减轻MIRI,其作用可能与其抑制NF-κB的激活及炎症反应有关。
Objective: To evaluate the effect of TDZD-8, a glycogen synthase kinase-3β (GSK-3β) inhibitor, on acute myocardial ischemia / reperfusion injury (MIRI) in rats and its role in down-regulating NF-κB and inhibiting inflammation related. Methods: Sixty healthy male Sprague-Dawley rats were randomly divided into 2 groups: ischemia / reperfusion (I / R) group, I / R + TDZD group, vehicle / V group and sham group . Local ischemia in rats 30 min, reperfusion 3 h. The area of myocardial infarction was calculated by TTC staining. The changes of neutrophil infiltration and inflammatory cytokines (TNF-α and IL-6) in myocardium were evaluated by HE staining and ELISA. The expressions of NF-κB, GSK -3β phosphorylation levels. Results: TDZD-8 significantly reduced myocardial infarct size and myocardial neutrophil infiltration, and inhibited NF-κB activation as well as myocardial TNF-α and IL-6 concentrations (P <0.01). Conclusion: GSK-3β inhibitor TDZD-8 can reduce MIRI, which may be related to the inhibition of NF-κB activation and inflammation.