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目的:模拟人类中风病疾病过程,界定缺血性卒中后遗症大鼠模型。方法:电凝法制成大鼠MCAO模型,以BWT评分法自MCAO术后3天开始动态观察大鼠四肢精细运动功能积分;结合同期脑组织病理形态学改变;免疫组化方法观察病灶区及周围反应区生长相关蛋白(GAP-43)、突触素P38(SYN)、细胞骨架蛋白(MAP-2、NF200)、氧化还原因子-1(Ref-1)的表达以及神经细胞凋亡的变化;ELISA法观察血清神经元特异性烯醇化酶(NSE)的动态变化等,研究上述变化的特点及其与病理过程间的关系。结果:神经行为学观察表明大鼠MCAO术后3～7天运动功能恢复较快,4周内仍有较明显的改善,5周后功能恢复曲线呈现平台势线;病理形态学显示MCAO术后4周病变区形成致密瘢痕组织,5周后病灶区及其周边形成异形胶样变性;免疫组化和生化检测结果提示MCAO术后4周内是模型大鼠进行组织结构修复和功能恢复的时间。结论:大鼠MCAO5周后为缺血性卒中后遗症大鼠模型。
OBJECTIVE: To simulate the course of human stroke disease and define the sequelae of ischemic stroke in rats. Methods: The rat MCAO model was established by electrocoagulation. BWC score was used to observe the fine motor function of limbs in rats from 3 days after MCAO. Pathological changes of brain tissues were observed with immunohistochemistry. (GAP-43), the expression of synaptophysin P38 (SYN), cytoskeletal protein (MAP-2, NF200) and redox factor-1 The dynamic changes of serum neuron specific enolase (NSE) were observed by ELISA. The characteristics of these changes and their relationship with pathological process were studied. Results: The neurobehavioral observation showed that motor function recovered rapidly in rats 3 ~ 7 days after MCAO, and still improved obviously in 4 weeks. After 5 weeks, the functional recovery curve showed a plateau potential. Morphology showed that MCAO At 4 weeks after operation, dense scar tissue was formed in the lesion area. At 5 weeks, the lesion area and its peritoneum formed irregular plastic degeneration. The results of immunohistochemistry and biochemical examination indicated that the model rats were repaired and function recovered within 4 weeks after MCAO . CONCLUSION: Rat MCAO is a rat model of sequelae of ischemic stroke after 5 weeks.