摘要
目的:探讨过氧化物酶体增殖物激活受体α(PPARα)和其配体非诺贝特在急性心肌缺血性损伤中的作用及其机制。方法:30只雄性纯系Wistar大鼠随机分为3组,每组10只:①正常对照组(control);②异丙肾上腺素损伤组(Iso)采用腹腔内注射异丙基肾上腺素复制急性心肌缺血损伤的动物模型;③非诺贝特组(FF)在预先给予非诺贝特的基础上复制异丙基肾上腺素致急性心肌缺血损伤的动物模型。生化酶学方法测定大鼠血清心肌酶学(CK,LDH);紫外分光光度法测定心肌组织中髓过氧化物酶(MPO)的酶活力;酶联免疫吸附实验(ELISA)测定血清中TNF-α的浓度;RT-PCR方法测定PPARα mRNA的表达水平。结果:Iso组血清心肌酶CK和LDH的含量和心肌组织中髓过氧化物酶(MPO)的酶活力显著高于对照组,心肌炎症反应较重,血清TNF-α浓度也增高,同时心肌组织中PPARα mRNA表达水平明显低于对照组;FF组与Iso组比较,前者血清心肌酶CK和LDH的释放受到抑制低于后者,心肌组织中髓过氧化物酶MPO的酶活力和血清TNF-α浓度均低于Iso组,但心肌组织中PPARα mRNA表达水平高于Iso组(P<0.01)。结论:PPARα参与急性心肌缺血性损伤中的炎症反应;PPARα配体非诺贝特可能是通过激活PPARα,减轻炎症反应,对缺血心肌具有保护作用。
AIM： To investigate the effects and mechanism of PPARα and its actor fenofibrate （FF） on injury caused by myocardial ischemia in rats. METHODS： The experimental animals were randomly divided into control group, isoprenaline （ISO） group and FF group. Actue myocardial injury caused by intraperitoneal injection of isoprenaline to induce ischemia was established. The following changes were measured： the level of creatine kinase （CK） and lactic dehydrogenase （LDH） in serum, the activity of myocardial myoperoxidase （ MPO）, the changes of serum TNF - α by ELISA and the level of PPARα mRNA by RT - PCR. RESULTS ： As compared with ISO group, FF depressed significantly the release of CK and LDH in serum, alleviated significantly myocardial inflammation, depressed the changes of serum TNF - α, obviously increased the level of PPARα mRNA in the isoprenaline - induced injury in rat heart （ P 〈 0.01 ）. CONCLUSION： These results suggest that FF may inhibit myocardial inflammation and exert protective effects on the acute myocardial ischemia injury induced by ISO in rats. PPARα may mediate the modulation of the inflammatory reaction.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2007年第3期525-528,共4页
Chinese Journal of Pathophysiology
关键词
受体
过氧化物酶增殖剂
异丙肾上腺素
心肌缺血
炎症
Receptors, peroxisome proliferator
Isoproterenol
Myocardial ischemia
Inflammatory
