当归对大鼠缺血再灌注心肌HSP70和NF-κB的影响

目的 :观察当归注射液对缺血再灌注 (I/R)过程心肌热休克蛋白 70 (HSP70 )和核转录因子κB(NF κB)表达的影响 ,探讨当归抗心肌缺血再灌注损伤的可能作用机理。方法 :4 5只SD大鼠随机分成 3组 (每组n =15 ) :假手术组 (Ⅰ组 ) ,缺血再灌注组 (Ⅱ组 ) ,当归治疗组 (Ⅲ组 ) ,建立在体心肌缺血再灌注动物模型。每组 5只动物再灌注 4 0min用化学扩增法测定SOD活性 ,TBA法测定MDA含量 ;10只动物再灌注 12 0min测定HSP70免疫组化SP法观察心肌细胞HSP70蛋白表达 ,用ESMA法观察NF κB的变化 ,在电镜下观察心肌细胞的超微结构。结果 :再灌注前注射当归注射液显著降低了再灌注心肌MDA水平 (P <0 .0 1) ,增强了SOD活性 (P <0 .0 1)和HSP70的表达 (P <0 .0 1) ,减低NF κB的活性 ,同时减轻了心肌的超微结构损伤。结论 :当归注射液可通过抗氧化作用、增加HSP70的表达和减低NF κB的活性发挥抗心肌缺血再灌注损伤 ,对心肌有明显的保护作用。

Effect of Intravenous Angelica on HSP70 and NF-κB During Myocardial Ischemia and Reperfusion Injury in Rats

Objective: To test the hypothesis that adminstration of angelica pro-injection before ischemia and reperfusion protects myocardium. Methods: Myocardial ischemia and reperfusion model was done using Sprague-Dawley rats subjected to 30 minutes occlusion of left coronary artery followed by 40 min or 120 min reperfusion. Group Ⅰ (control group) was the sham operation group. Group Ⅱ was ischemia and reperfusion group. Group Ⅲ was angelica treatment group. Malondialdehyde (MDA) content was detected by TBA and superoxide dismutase (SOD) activity was measured by chemical amplification. The expressions of heat shock protein-70 (HSP70) were measured by immunohistochemical techinique. The myocardial ultrastructure was observed under electronic microscope. Nuclear factor-kappaB(NF-κB) activation was determined by electrophoretic mobility shift assay(EMSA). Results: MDA content of myocardium was reduced singificantly in group Ⅲ (P<0.01), but singificantly increased in groupⅡ(P <0.01). SOD activity and HSP70 expression of myocardium in group Ⅲ were higher than those of groupⅡ(P<0.01). Under electronic microscope, myocardial ultrastuctral in groups Ⅲ was singificantly improved in comparision with groupⅡ. NF-κB activation was reached its maximum increase in group Ⅱ(P<0.01), ant it was remarkably decreased in group Ⅲ(P<0.01). Conclusion: Angelica might protect the myocardium from ischemia-reperfusion injury via the improvement of HSP70 expression and the downregulation of NF-κB.