摘要
目的 探讨肿瘤坏死因子-α(TNF-α)预处理对大鼠脑缺血再灌注损伤的影响及可能机制。方法 采用线栓法制作大鼠局灶性脑缺血再灌注模型,并予以改良。在脑缺血前48小时,给大鼠小脑延髓池内注射不同剂量的 TNF-α(0.05μg,0.5μg,1.0μg)或PBS液,缺血2小时后再灌注22小时,处死大鼠,进行脑梗死体积测定、病理学观察及免疫组化法检测胶质纤维酸性蛋白(GFAP)、细胞间粘附分子-1(ICAM-1)蛋白表达情况。结果 与对照组相比,0.05μg组各指标无显著差异(P>0.05),0.5μg组及1.0μg组脑梗死体积显著减小(均P<0.001),脑组织变性坏死程度减轻,GFAP阳性的星形胶质细胞减少(均P<0.001),ICAM-1阳性的血管内皮细胞减少(均P<0.001)。结论 TNF-α可诱导脑缺血耐受,与星形胶质细胞的修复作用无关,而与ICAM-1表达下调、减轻再灌注后炎症反应有关,TNF-α诱导脑缺血耐受有剂量依赖性。
Objective To study the effect of TNF-α pretreatment on cerebral ischemia-reperfusion injury and possible mechanism in rat. Methods Rat focal brain ischemic model of middle cerebral artery occlusion(MCAO) was made by using inserting thread method. Different doses of TNF-α or PBS was injected intracisternally 48 hours before ischemia. After 2 hours ischemia and 22 hours reperfusion, the rats were killed. Then, the percent of cerebral infarction volume was measured, pathological change was observed, GFAP and ICAM-1 expression were inspected by immunohistochemistry. Results Compared with control group,TNF-α 0.05μg pretreatment group displayed no difference( P > 0.05) ;TNF-α 0.5 μg and TNF-α 1.0 μg pretreatment groups showed reduced volume of lesion(all P < 0.001) .lightened tissue damage,less GFAP and ICAM-1 expression( all P < 0.001) . Conclusion TNF-α could induce cerebral ischemic tolerance and the effect didn't depend on repair of astrocyte, but relied on relieved inflammation characterized by the expression of ICAM-1 . In addition,this effect was doses-dependent.
出处
《临床神经病学杂志》
CAS
2003年第3期153-155,共3页
Journal of Clinical Neurology
基金
2002年黑龙江省科委攻关课题(课题号GB01C125-01)
