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目的:探讨灯盏花联合预适应对兔缺血再灌注心肌肿瘤坏死因子α(TNF-α)、核因子-κB(NF-κB)的影响。方法:采用新西兰大白兔体内心肌缺血再灌注模型,36只动物随机分为假手术组(Sham组)、缺血再灌注组(IR组)、缺血预适应组(IP组)、灯盏花素联合缺血预适应组(BI组)。各组分别进行心肌酶学[肌酸激酶(CK)及乳酸脱氢酶(LDH)]检查,并采用伊文思蓝(EB)/氯化三苯基四氮唑(TTC)测定梗死面积,用免疫组化法检测TNF-α及NF-κB蛋白表达水平。结果:IR、IP及BI组较Sham组均有明显的心肌梗死(P<0.01),IP、BI组较IR组能够明显缩小心肌梗死面积(P<0.01),BI组较IP组疗效显著(P<0.05);IR、IP及BI组心肌酶较Sham组均明显升高(P<0.01),IP、BI组各时间点CK和LDH均较IR组明显降低(P<0.01),且BI组较IP组降低更明显(P<0.05);IR、IP及BI组较Sham组TNF-α及NF-κB蛋白表达均明显增加(P<0.01);IP组、BI组TNF-α及NF-κB蛋白表达均较IR组显著较少(P<0.01),且BI组较IP组更明显(P<0.05)。结论:缺血预适应及灯盏花素联合预适应均显著缩小心肌梗死面积,降低心肌酶,减少心肌细胞内TNF-α、NF-κB蛋白的表达。
Objective: To investigate the effect of Erigeron breviscapus preconditioning on tumor necrosis factor-α (TNF-α) and nuclear factor-κB (NF-κB) in rabbits with ischemia-reperfusion injury. Methods: New Zealand white rabbits model of myocardial ischemia reperfusion, 36 animals were randomly divided into sham operation group (Sham group), ischemia reperfusion group (IR group), ischemic preconditioning group (IP group) Superimposed ischemic preconditioning group (BI group). Myocardial enzymology [CK and LDH] was performed in each group, and infarct area was measured by Evans blue (EB) / triphenyltetrazolium chloride (TTC) Immunohistochemistry was used to detect the expression of TNF-α and NF-κB. Results: Compared with Sham group, the myocardial infarct size was significantly decreased in IR, IP and BI groups (P <0.01), and the myocardial infarct size was significantly reduced in IP and BI groups as compared with IR group (P <0.01) P <0.05). The levels of myocardial enzymes in IR, IP and BI groups were significantly higher than those in Sham group (P <0.01), while CK and LDH in IP and BI groups were significantly lower than those in IR group (P <0.01) (P <0.05). The expression of TNF-α and NF-κB protein in IR, IP and BI groups were significantly increased compared with Sham group (P <0.01). The levels of TNF-α and NF (P <0.01), and the BI group was more obvious than the IP group (P <0.05). Conclusions: Both ischemic preconditioning and breviscapine preconditioning can significantly reduce myocardial infarct size, decrease myocardial enzymes and decrease the expression of TNF-α and NF-κB in cardiomyocytes.