依达拉奉抑制血管性痴呆大鼠脑组织环氧化酶2及NFκB表达.doc

依达拉奉抑制血管性痴呆大鼠脑组织环氧化酶2及NFκB表达 　作者：蔡志友 晏勇 张骏 晏宁 王咏龙 吴芳 黄华 张建刚 【摘要】 目的 观察依达拉奉对血管性痴呆(VD)大鼠行为学和脑组织环氧化酶2（COX2）、核转录因子κB（NFκB）表达的影响，探讨依达拉奉对VD脑保护作用机制。方法 Wistar大鼠随机分为：正常组、假手术组、痴呆模型组（模型组）、依达拉奉治疗组（治疗组）。水迷宫和穿梭箱实验检测行为学特征；免疫组织化学法和蛋白质免疫印迹法检测大鼠脑组织COX2、NFκB的表达，用图象分析仪测定光密度(OD)值。结果 治疗组大鼠的前后两次跳台实验的检测结果差异显著(P＜0.01)，治疗组的行为学症状较模型组明显改善。NFκBp65和COX2阳性细胞百分率治疗组较正常组、假手术组明显增高（P＜0.01），较模型组明显降低（P＜0.01），NFκBp65和COX2 OD值，治疗组较正常组、假手术组明显降低（P＜0.01），较模型组明显增高（P＜0.01）。结论 依达拉奉能明显改善VD大鼠的行为学症状、降低大鼠脑组织NFκBp65和COX2表达，依达拉奉能够通过抑制大鼠脑组织NFκBp65和COX2表达途径发挥其脑保护作用。 【关键词】 血管性痴呆；依达拉奉；环氧合酶2；核转录因子κB 　　【Abstract】 Objective To observe the effects of edaravone on praxiology changes and the expressions of cyclooxygenase2 (COX2), nuclear factorkappa B (NFκB) in brain of vascular dementia (VD) rats，to study the neuroprotective mechanisms of edaravone. Methods Wistar rats were randomly divided into normal, sham, VD model and edaravone treatment groups. Praxiology changes were tested by Morris water maze and shuttle box. The expressions of COX2, NFκB were measured by immunohistochemistry and Western blot. The OD values of COX2, NFκB were measured by imaging analysis. Results The praxiology symptoms were improved in edaravone treatment group compared with model group. The percentages of COX2 positive cells and NFκB p65 positive cells in edaravone treatment group were increased than those in normal and sham groups(P＜0.01), and decreased than those in model group(P＜0.01). The OD values of COX2 and NFκB in edaravone treatment group were decreased than those in normal and sham groups(P＜0.01) and increased than those in model group(P＜0.01). Conclusions Edaravone can improve praxiology symptom and downregulate expressions of COX2, NFκB in VD rats. Edaravone can exert cerebral protection by inhibiting the COX2 and NFκB pathway. 　　【Key words】 Vascular dementia; Edaravone; Cyclooxygenase2; Nuclear factorkappa B 　　细胞凋亡是血管性痴呆（VD)重要的病理生理机制，痴呆程度和细胞凋亡有着直接的联系，同时，细胞凋亡也参与脑缺血损伤机制过程〔1〕。环氧化酶2(COX2)和核转录因子κB(NF