摘要
目的:探讨定心方防治大鼠心肌缺血再灌注损伤的作用机制。方法:60只SD大鼠随机分为5组:假手术组、模型组、肿瘤坏死因子α(tumornecrosisfactor-α,TNF-α)抗体组、定心方小剂量组和定心方大剂量组,每组12只。利用结扎、放松左冠状动脉的方法制作大鼠心肌缺血再灌注损伤模型。用放射自显影激酶活性测定心肌中p38丝裂原激活蛋白激酶(p38mitogen-activatedproteinkinases,p38MAPK)活性。用2,4二硝基苯肼显色法测定血清乳酸脱氢酶(lactatedehydrogenase,LDH)活性。用免疫酶联吸附法(ELISA)检测心肌内TNF-α含量。结果:定心方大、小剂量组均能不同程度地提高再灌注后平均动脉压(meanarterialpressure,MAP),减少血清LDH的活性。MI/R模型组大鼠心肌中TNF-α的含量(pg/g)显著高于假手术组(1120±111和165±16;t=23.483,P<0.01);与模型组相比,TNF-α抗体组、定心方大、小剂量组均能显著降低心肌中TNF-α含量,分别为312±25,515±54,843±86;差异有显著性意义(t=18.341,23.142,5.554,P均<0.01)。MI/R模型组大鼠心肌中p38MAPK活性(nkat/g)显著高于假手术组(90.01±2.88和16.67±0;t=44.00,P<0.01);TNF-α抗体组心肌中p38MAPK活性(93.35±2.55)与模型组无显著性差异(t=0.866,P>0.05);定心方大。
AIM:To study the mechanisms of dingxin recipe in prevention and treatment of m yocardial ischemia reperfusion injury. METHODS:Sixty SD rats were randomly divided into five groups:sham operation gr oup,model group,tumor necrosis factor-alpha (TNF-α) group,antibody group;low dose and high dose dingxin recipe groups.Rat models of myocardial ischemia reper fusion in rats were established by ligating and loosing the left coronary arteri es.Activity of p38 mitogen-activated protein kinase(p38 MAPK) was measured by a utoradiography kinase activity,while that of lactate dehydrogenase(LDH) was assa yed by using spectrophotometric procedures.Enzyme-linked immunosorbent assays(E LISA) was used to detect the content of TNF-α. RESULTS:Dingxin recipe of low and high doses could improve the mean arterial p ressure(MAP) after reperfusion on different degree,and decrease the activity of LDH.After myocardial ischemia reperfusion,TNF-αcontent(pg/g) of the model grou p(1 120±111) was significantly higher than that of the sham operation group(165 ±16) (t=23.483,P< 0.01);Compared with the model group,myocardial TNF-αcontent s of the TNF-αantibody group(312±25),high and low dose dingxin recipe groups[ (515±54) and(843±86)] were markedly reduced(t=18.341,23.142,5.554,P< 0.01). My ocardial p38 MAPK activity(nkat/g) of the model group(90.01±2.88) was significa ntly higher than that of the sham operation group(16.67±0)(t=44,P< 0.01);while not obviously different from that of the TNF-αantibody group(93.55±2.55)(t=0. 866,P >0.05);and significantly high than those in the high and low dose dingxin recipe groups[(58.34±3.33) and(68.35±3.33)](respectively,t=32.909,6.245,P< 0.0 5). CONCLUSION:Dingxin recipe can reduce the formation of myocardial TNF-αthroug h regulating p38 MAPK signal transduction,so as to protect myocardial cells and relieve myocardial ischemia reperfusion in rats.
出处
《中国临床康复》
CSCD
2004年第15期2882-2884,共3页
Chinese Journal of Clinical Rehabilitation
基金
国家中医药管理局基金资助项目(30271573)~~
