阿托伐他汀钙对实验性脑缺血再灌注后炎症反应的影响

Effects of Atorvastatin on Inflammatory Response of Cerebral Ischemia—Reperfusion Injury in Rats

目的研究阿托伐他汀钙对大鼠大脑中动脉缺血再灌注后脑组织中核因子κBp56、细胞间粘附分子1蛋白表达及炎症细胞渗出的影响。方法采用大脑中动脉线栓法制备局灶性脑缺血再灌注模型,参考Longa5分制法在动物麻醉清醒后进行评分,应用免疫组织化学检测核因子κBp56和细胞间粘附分子1蛋白表达,运用HE染色观察多形核白细胞浸润的情况。结果他汀组与缺血组比较,大鼠缺血侧脑组织中核因子κBp56蛋白和细胞间粘附分子1蛋白表达减少(P<0.05),多形核白细胞渗出减少(P<0.05),神经病学评分也减少(P<0.05)。结论阿托伐他汀钙能抑制缺血再灌注后脑组织中核因子κBp56和细胞间粘附分子1蛋白表达,从而减少炎症细胞渗出,抑制大鼠实验性脑缺血再灌注后炎症反应,最终减轻其缺血再灌注损伤。

Aim To investigate ff the atorvastatin calcium protects the brain against injury induced by ischemia/reperfusion（ I/R） and its impact on the expression of nuclear factor-tcBp56（NF-κBp56） and intercellular adhesion molecule- 1 （ICAM-1 ）. Methods Rats were subjected to cerebral I/R injury through the occlusion of the middle cerebral artery. Neurological deficits were determined by Longa＇s score. The expression of ICAM-1 and NF-κB were detected by immuno-histochemical analysis. The effusion of polymorphonuclear leucocytes （PMNLs） in brain tissue was evaluated by HE staining. Results In group I/R ＋ stalin, contrasting to group I/R, the expression of ICAM-1 and NF-κB were decreased significantly （ P 〈 0.05） ; the Longa＇s score were lower （ P 〈 0.05 ） ; and the effusion of PMNLs were inhibited （ P 〈 0.05 ）. Conclusion Atorvastatincalcium has protective effects on the brain after experimental stroke and its probable mechanism involves the decreased expression of NF-κBp56 and ICAM-1.