摘要
目的:研究过氧化物酶体增生物激活受体γ(PPARγ)激动剂吡格列酮预处理对大鼠脑缺血再灌注损伤的影响,探讨PPARγ在脑缺血再灌注损伤中的作用。方法:选用健康SpragueDawley(SD)大鼠72只,随机分为假手术组、对照组和吡格列酮组。采用大鼠大脑中动脉闭塞2h再灌注模型,于缺血再灌注损伤后24h,进行神经功能缺陷评分监测神经功能缺损情况;通过2,3,5,-氯化三苯基四氮唑(TTC)染色测定脑梗死体积;通过干湿重法检测脑水含量;通过TUNEL方法,观察各实验组鼠脑缺血半暗带神经细胞的凋亡。结果 :与对照组相比,缺血再灌注损伤后24h吡格列酮组的神经功能缺陷评分(P<0.05)、脑梗死面积(P<0.05)、脑水含量(P<0.01)和缺血半暗带神经细胞凋亡(P<0.01)均明显低于对照组。结论:PPARγ激动剂吡格列酮对大鼠缺血再灌注脑损伤有明显的保护作用,抗凋亡作用可能是PPARγ发挥保护作用的机制之一。
Objective ：To investigate the role of peroxisome proliferator activated receptor γ（PPARTγ）in cerebral ischemic injury by PPAR7 agonist pioglitazone treating in rats. Methods： One seventy-two Sprague-Dawley （SD） rats were randomly divided into sham group, middle cerebral artery occlusion （MCAO） group and pioglitazone treatment group. At 24h after ischemia reperfusion injury, neurological impairment was evaluated by neurological deficit score （NDS）, infarct volume was measured by dUTP nick-end labeling 2,3,5, triphenyltetrazolium chlo- ride （TTC） staining, brain water content was measured by dry and wet weights of brain, and neuronal apoptosis in the ischemic brain tissue was assessed in situ by terminal deoxynucleotide transferase-mediated （TUNEL） staining at 24h after ischemic brain injury. Results ：Compared with MCAO group rats, NDS（P〈0.05）, infarct volume（P〈0. 05）, brain water content（P〈0.01） and neuronal apoptosis（P〈0.01） in the ischemic brain tissue were significantly lower than those in GW501516 pretreatment group rats at 24h after ischemic brain injury, respectively. Conclusion： pioglitazone, a PPARyagonist, has a neuroprotective effect on ischemic brain injury in rats, and the antiapoptosis effect of pioglitazone may contribute to a beneficial effect against ischemic brain injury.
出处
《陕西医学杂志》
CAS
2013年第12期1574-1575,1580,共3页
Shaanxi Medical Journal
基金
陕西省自然科学基金(2010JM4032)
