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目的探讨脂多糖(LPS)预处理对大鼠心肌缺血再灌注(I/R)损伤的保护作用及机制。方法建立大鼠在体心肌I/R模型,24只SD大鼠随机分为3组:假手术组(Sham组),缺血再灌注组(I/R组),LPS预处理组(ET组)。HE染色观察各组心肌形态学改变,RT-PCR法检测心肌组织中白细胞介素-1受体相关激酶-4(IRAK-4)mR-NA水平,Western-Blot法检测心肌组织IRAK-4蛋白水平,免疫组化方法检测心肌组织中NF-κB的表达,ELISA法检测血清TNF-α含量。结果 HE染色提示ET组心肌细胞损伤较I/R组明显减轻。ET组及I/R组心肌组织IRAK-4mRNA水平及蛋白水平、NF-κB及血清TNF-α含量明显高于Sham组(均P<0.01),并且ET组的表达水平又明显低于I/R组(P<0.01)。结论抑制IRAK-4表达进而抑制NF-κB及TNF-α的表达,可能是LPS预处理减轻心肌I/R的重要机制之一。
Objective To investigate the protective effect and mechanism of lipopolysaccharide (LPS) preconditioning on myocardial ischemia-reperfusion (I / R) injury in rats. Methods Twenty-four Sprague-Dawley rats were randomly divided into 3 groups: Sham group, I / R group, LPS preconditioning group (ET group) ). The morphological changes of myocardium were observed by HE staining. The level of mR-NA in myocardium was detected by RT-PCR. The expression of IRAK-4 protein in myocardium was detected by Western-Blot. The expression of NF-κB in myocardium was detected by immunohistochemistry and the content of TNF-α in serum was detected by ELISA. Results HE staining showed that the injury of cardiomyocytes in ET group was significantly less than that in I / R group. The levels of IRAK-4 mRNA and protein, the levels of NF-κB and TNF-α in myocardium of ET and I / R group were significantly higher than those of Sham group (all P <0.01), and the expression level of ETAK was significantly lower than that of I / R group (P <0.01). Conclusions Inhibition of IRAK-4 expression and the inhibition of NF-κB and TNF-α expression may be one of the important mechanisms of LPS pretreatment to reduce myocardial I / R.