丁苯酞对Wistar大鼠血管性痴呆模型中海马区OX-42的影响

The effect of NBP on the expression of OX-42 of hippocampus in wistar rats with vascular Dementia

目的 :通过检测Wistar大鼠血管性痴呆模型中小胶质细胞表面补体Ⅲ型受体OX-42在脑海马组织中的动态变化,探讨丁苯酞在血管性痴呆中的作用。方法 :双侧颈总动脉永久结扎术(2-VO)建立Wistar大鼠血管性痴呆模型。设立正常对照组、假手术组、VD模型组、药物干预组。水迷宫试验对大鼠进行学习和记忆成绩测试。应用免疫组织化学法方法检测OX-42的表达。结果 :模型组大鼠学习和记忆成绩下降,海马区OX-42的表达较正常对照组、假手术组均明显增加;药物干预组大鼠学习记忆能力明显改善,海马区OX-42的表达下降,与模型组比较差异有统计学意义。结论 :慢性脑缺血血管性痴呆大鼠海马区OX-42表达升高;丁苯酞可能通过抑制了血管性痴呆大鼠海马区OX-42的表达,从而改善大鼠的学习记忆能力。

Objective To investigate the dynamic variation of OX-42 in hippocampus tissue after vascular dementia(VD) model in Wistat rats, to explore their effects in vascular dementia. To investigate the effects of Butylphthalide(NBP)on OX-42 after VD model in rats, and clarify the possible mechanism of NBP. Methods The vascular dementia modelin Wistar rats were established bypermanentbilateral commoncarotid arteryocclusion method. Wistar rats were divided into 4 groups:normal group, sham-operated group, VD model groupand NBP treatment group. Then the learning and memory capabilities of rats were tested by Morris water maze. Meanwhile, the expression of OX-42were measured with methods of immunohistochemistry. Results Compared with the normal group and sham-operated group, the abilities of learning and memory apparently decresed in VD model group, and the expression of OX-42 significantly increased in VD model group. Besides, NBP treatment groupsignifi-cantlyimproved learning and memory abilities, and compared with the VD model group, the expression of OX-42 significant-lyreduced in NBP treatment group. Conclusion OX-42 expression were significantly increased in hippocampusof chronic cer-ebral ischemia rats. Butylphthalidemight reduced expression of OX-42, and could improve learning and memory abilities of VD rats.