亚低温对局灶性脑缺血再灌注大鼠过氧化物酶体增殖物激活受体γ表达的影响

The Effects of Mild Hypothermia on the Expression of Peroxisome Proliferator-Activated Receptor γ in Rats Brains after Focal Cerebral Ischemia and Reperfusion

目的:研究亚低温对局灶性脑缺血再灌注大鼠过氧化物酶体增殖物激活受体(PPARγ)表达的影响,进一步探讨亚低温对局灶性脑缺血再灌注损伤脑保护作用的机制。方法:线拴法建立大鼠大脑中动脉阻塞再灌注模型,分为假手术组、假手术+亚低温组、模型组及模型+亚低温组。应用Western blotting和免疫组化技术分别检测再灌注后不同时相缺血侧皮层PPARγ蛋白的含量和空间分布。结果:假手术组、假手术+亚低温组PPARγ蛋白有少量表达。脑缺血2h再灌注3h,PPARγ蛋白表达开始增加,随再灌注时间的延长表达量逐渐增加,至再灌注24h达高峰,然后明显减少,再灌注72h时仍高于假手术组的水平。每一相同再灌注时间点,模型+亚低温组PPARγ蛋白表达量均明显低于模型组。结论:亚低温可通过抑制PPARγ的表达上调而发挥一定程度的脑保护作用。

Objective： To investigate the effects of mild hypothermia on the expression ofperoxisome proliferator-activated receptor γ（PPARγ） in rats brains after focal cerebral ischemia and reperfusion and discuss the molecular mechanisms of the neuroprotecfive effects of mild hypothermia. Methods ：Focal cerebral ischemia and reperfusion model was made by an intraluminal filam ent embolism of the middle cerebral artery. The adult rats were randomly divided into four groups： sham-operated group, shamop crated plus mild hypothermia group, models group, and models plus mild hypothermia group. The expression of PPAR γprotein in ischemie cortex at different phases after reperfusion was assessed by Western blotting and immunohistochemistry stain. Results： There is low expression of PPAR γ protein in rats of sham-operated group, sham-operated plus mild hypothermia group. PPAR γ protein began to increase after 2 h of cerebral ischemia and 3 h of reperfusion, increased gradually with the progress of reperfusion and peaked at 24 h of reperfusion, and decreased remarkably, was still more than that of the sham-operated group at 72 h after reperfusion. Compared with models group, PPAR γ protein markedly decreased in models plus mild hypothermia group. Conclusion： Partial inhibition of the up regulation ofPPAR γ after focal cerebral ischemia and reperfusion is responsible for the mechanisms ofneuroprotective effects of mild hypothermia.