摘要
目的观察大鼠局灶性脑缺血再灌注损伤(CIRI)后杏仁核和海马环氧酶-2(COX-2)、5-脂氧酶(5-LO)和核因子-κB(NF-κB)的表达情况,探讨其损伤机制。方法线栓法制备大鼠大脑中动脉栓塞2h/再灌注24h模型。免疫组织化学法检测杏仁核和海马COX-2、5-LO和NF-κB蛋白表达,计数COX-2、5-LO和NF-κB阳性细胞数,Motic Images Advanced3.0图像分析系统作半定量分析。结果CIRI后大鼠杏仁核和海马COX-2、5-LO和NF-κB阳性细胞计数明显增高(P<0.001),平均灰度值显著下降,表达增强(P<0.001)。结论CIRI后大鼠杏仁核和海马区域的COX-2、5-LO和NF-κB表达增强,继而引发后续反应,介导神经损伤。
Objective To investigate the changes of the expression of cyclooxygenase-2(COX-2),5-hpoxygenase(5-LO) and nuclear factor-κB(NF-κB) protein after the focal cerebral ischemia-reperfusion injury(CIRI) in rats. Methods The model of focal CIRI was induced by reversible middle cerebral artery occlusion by inserting a thread through internal carotid artery for 2 hours' occlusion followed by 24 hours'reperfusion. Use immunohistochemistry technique to examine the expression level of COX-2, 5-LO and NF-κB proteins in amygdala and hippocampus. Moreover, the positive staining cells of NF-κB prote the positive ins were calculated in 10 × 40 field of vision via optic microscope. Results COX-2, 5-LO and The expression of staining cells of COX-2, 5-LO and NF-κB proteins were increased significantly after CIRI [amygdala and hippocampus.COX-2(28.8±3.2), (30.4±2.9) ± 5-LO(30.7±3.0), (32.8±3.5) ± NF-κB (27.9±1.3), (25.4±0.9), (P±0.001)]. The expression of COX-2, 5-LO and NF-κBproteins are significantly increased after focal CIRI both in amygdala and hippocampus. Then it will exert consequent reaction and cause focal neuronal damage.
出处
《福建医科大学学报》
2007年第3期207-210,共4页
Journal of Fujian Medical University
基金
福建省自然科学基金资助项目(C0110010)