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目的初步探讨腺苷后适应对大鼠缺血再灌注损伤心肌的保护作用及机制。方法48只健康雄性SD大鼠随机分为4组:假手术组(Sham组)、缺血再灌注组(IR组)、缺血后处理组(IPTC组)及腺苷后适应组(ADOP组),每组12只,建立大鼠在体心肌缺血再灌注损伤模型。实验终点测定心肌梗死面积(TTC染色),心肌核因子-κB(NF-κB)mRNA的表达水平(RT-PCR),同时观察心肌组织中白细胞介素-6(IL-6)、丙二醛(MDA)及超氧化物歧化酶(SOD)的含量变化,并行心肌组织病理学检查。结果Sham组心肌组织形态改变不明显,IR组心肌损伤较重,IPTC组及ADOP组中心肌组织病理学损伤较IR组明显减轻。与IR组比较,ADOP组的心肌梗死面积、NF-κBmRNA的表达水平及IL-6、MDA含量明显降低(P<0.01),而SOD含量则显著升高(P<0.01);而ADOP组与IPTC组相比,除NF-κBmRNA的表达及IL-6的分泌稍许降低(P<0.05)外,其他均无统计学差异(P>0.05)。结论腺苷后适应可通过抑制再灌注后氧自由基的过量生成及NF-κB活化所诱导的早期炎症反应,增强心肌抗氧化能力,从而发挥保护效应。
Objective To investigate the protective effect and mechanism of adenosine postconditioning on myocardial ischemia-reperfusion injury in rats. Methods Forty-eight healthy male Sprague-Dawley rats were randomly divided into 4 groups: Sham group, IR group, IPTC group and ADAMP group ), 12 rats in each group. The rat model of myocardial ischemia-reperfusion injury was established. The myocardial infarct size (TTC staining) and the expression of NF-κB mRNA (RT-PCR) were determined at the end of the experiment. The levels of interleukin-6 (IL- (MDA) and superoxide dismutase (SOD) content changes, parallel myocardial histopathological examination. Results The morphological changes of myocardium in Sham group were not obvious. The myocardial injury in IR group was heavier. The pathological damage of myocardial tissue in IPTC group and ADOP group was less than that in IR group. Compared with the IR group, the myocardial infarct size, NF-κB mRNA expression and the levels of IL-6 and MDA in ADOP group were significantly decreased (P <0.01), while the SOD content was significantly increased (P <0.01) Compared with IPTC group, there was no significant difference except NF-κB mRNA expression and IL-6 secretion (P> 0.05). Conclusions Adenosine possesses the protective effect by inhibiting the over-production of oxygen free radicals and the early inflammatory reaction induced by NF-κB activation after reperfusion, and enhancing the myocardial antioxidant capacity.