参附注射液对心肌缺血再灌注老年大鼠NF-κB p65及COX-2表达的影响

目的：探讨参附注射液对心肌缺血再灌注老年大鼠心肌组织NF-κB p65及COX-2的影响。方法：健康Wistar老年大鼠30只,18月龄,随机分为3组,假手术组（S组）、缺血再灌注组（I/R组）、参附注射液组（SF组）,每组10只。采用结扎左冠状动脉前降支制备心肌缺血再灌注模型。观察参附注射液对缺血再灌注老年大鼠血清中肌酸激酶同工酶（CK-KB）、天门冬氨基转移酶（AST）、乳酸脱氢酶（LDH）溢出量的影响;运用免疫组化法观察心肌缺血再灌注后心肌组织细胞中NF-κB p65的活性及COX-2的蛋白表达。结果：参附注射液能显著减少I/R老年大鼠血清中CK-KB、AST、LDH的溢出量。与S组比较,I/R组心肌组织NF-κB p65的活性增高,COX-2的蛋白表达明显增加（P〈0.05）。SF组中NF-κB p65、COX-2显著下降（P〈0.05）。结论：NF-κB p65和COX-2在心肌缺血再灌注中均有高水平表达,提示炎症参与了心肌缺血再灌注,机制可能是NF-κB p65通过对COX-2的转录调控发挥了重要作用;参附注射液可抑制NF-κB p65活性,降低COX-2的蛋白表达水平,减轻I/R心肌炎症反应,对心肌起保护作用。

Influence of ShenFu Injection on Expressions of NF-κB p65 and COX-2 in Aged Myocardial Ischemia Reperfusion Rat Model

Objective： To study the effects of ShenFu injection on expressions of NF-κB p65 and COX-2 in aged rat model with myocardial ischemia reperfusion. Method： Thirty aged wistar rats were randomly divided into three groups （n=10 each）： sham group（S group）; ischemia reperfusion group （FR group） and ShenFu group （SF group）. Mod- el with myocardial ischemia reperfusion was established through left anterior descending coronary artery ligation. In- fluence of ShenFu injection on spillage of creatine phosphokinase isoenzyme （CK-κB）, aspartate amino transferase （AST） and lactate dehydrogenase （LDH） in serum of aged rat with ischemia reperfusion were observed; activity of NF-κB p65 and expression of COX-2 in myocardial tissue after reperfusion were observed with immunohistochemical method. Result： Spillage of CK-κB, AST and LDH in serum of aged rats in I/R group decreased significantly. Com- pared with S group, activity of NF-κB p65 and protein expression of COX-2 improved in myocardial tissue of FR group （P〈0.05）. Above indexes in SF group dropped down remarkably. Conclusion： High level expression of NF-κB p65 and COX-2 demonstrated that inflammation participate in myocardial ischemia reperfusion. The mechanism might be NF-κB p65 play an important role through transferring and regulating COX-2. ShenFu injection can inhibit the ac- tivity of NF-xB p65, reduce expression level of COX-2, alleviate inflammatory reaction and protect myocardial muscle.