PPARγ激动剂罗格列酮对心肌缺血再灌注损伤的影响

目的：探讨过氧化物酶体增殖物激活受体γ（PPARγ）激动剂罗格列酮对心肌缺血再灌注损伤的影响及机制。 方法： 42只SD大鼠随机分为假手术组（14只）、I/R组（14只）和I/R+Ros组（14只）。应用结扎左冠状动脉60min，再灌注60min的方法制作心肌缺血再灌注模型；用NBT染色法判断心肌梗死面积；用放射免疫法测定血浆及心肌血管紧张素Ⅱ和醛固酮等指标。 结果： 与I/R组相比，I/R+Ros组降低心肌缺血再灌注后心肌梗死面积23.9%（P<0.05）；显著减轻心肌肿胀度（P<0.05）；明显抑制心肌血管紧张素Ⅱ、醛固酮及血浆血管紧张素Ⅱ水平（P<0.05）。 结论： PPARγ激动剂罗格列酮对心肌缺血再灌注损伤有保护作用，其机制可能与抑制心肌局部肾素-血管紧张素系统有关。

Effects of peroxisome proliferator-activated receptor γ activator rosiglitazone on myocardial ischemic-reperfusion injury in rats

AIM: To investigate the effect of peroxisome proliferator-activated receptor γ (PPARγ) activator rosiglitazone on myocardial ischemic-reperfusion injury in rats. METHODS: Forty-two SD rats were randomly divided into three groups： sham group (n=14)， I/R group (n=14) and I/R+rosiglitazone group (n=14). Myocardial infarct size was assessed by NBT staining. Plasma and myocardial angiotensin and aldosterone as well as plasma renin activity were detected by radioimmunoassay. RESULTS: Compared with I/R group， myocardial infarct size was reduced by 23.9% (P<0.05), myocardial edema was obviously lessened (P<0.05)； plasma and myocardial angiotensinⅡ as well as myocardial aldosterone were significantly inhibited in I/R+rosiglitazone group (P<0.05). CONCLUSION: PPARγ activator rosiglitazone provides a protective effect against myocardial ischemic-reperfusion injury in rats partly by inhibiting myocardial renin-angiotensin-aldosterone system.