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核移位的改变

被引：5

作者：

孙莉

徐艳炜

梁浩

孙国敏

程焱

机构：

[1] 天津医科大学总医院天津市神经病学研究所

来源：

中华神经科杂志 | 2010年 / 07期

关键词：

脑缺血; 再灌注损伤; PPARγ;

D O I：

暂无

中图分类号：

R743 [脑血管疾病];

学科分类号：

1002 ;

摘要：

目的观察过氧化物酶体增殖物激活受体γ(PPARγ)在脑缺血再灌注损伤中核移位的改变,并初步探讨该改变在脑缺血损伤中的意义。方法健康雄性SD大鼠制作大脑中动脉阻塞再灌注模型,缺血60min,再灌注4、8、24h。采用Western blot法、免疫组织化学和免疫荧光染色法观察PPARγ核移位的改变以及PPARγ激动剂和拮抗剂对PPARγ核移位的影响;同时,2,3,5-氯化三苯四唑(TTC)染色法观察脑梗死体积的改变。结果 (1)Western blot检测显示,脑缺血再灌注4h即引起PPARγ核蛋白增加,同时胞质蛋白减少,差异具有统计学意义。随再灌注时间的增加,PPARγ核移位呈时间依赖性增强。免疫组织化学和免疫荧光染色均显示,与假手术组48.3%相比,缺血再灌注24h胞核PPARγ阳性增加到80.3%,差异具有统计学意义(t=8.63,P=0.00)。(2)与单纯缺血再灌注组相比,PPARγ激动剂进一步增加PPARγ核蛋白表达,同时减少胞质蛋白表达,差异均具有统计学意义;相反,PPARγ抑制剂GW9662则降低核蛋白水平而增加胞质表达,差异均具有统计学意义。(3)经TTC染色显示,与单纯缺血再灌注组相比,PPARγ激动剂使脑梗死体积减少了48.40%(15.46±4.94与29.96±3.39,t=5.93,P=0.00);而PPARγ抑制剂则使脑梗死体积增加了58.95%(47.62±4.93与29.96±3.39,t=7.23,P=0.00)。结论脑缺血再灌注损伤使大鼠PPARγ核移位增加,该改变可能是脑组织的一种自我保护性反应。

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