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目的观察中药单体环维黄杨星D(CVB-D)对易卒中型肾血管性高血压大鼠(RHRSP)脑缺血再灌注不同时间脑组织生长相关蛋白-43(GAP-43)mRNA表达与细胞超微结构损伤的影响。方法采用环形银夹使SD大鼠的双侧肾动脉狭窄,制成RHRSP,再用线栓法制成一侧大脑中动脉闭塞(MCAO)模型。用原位杂交等方法观察CVB-D对脑缺血2h后复流1d、7d、14d、30d不同时间点大鼠脑组织GAP-43mRNA表达、水含量、梗死面积百分率、行为学评分及细胞超微结构的干预作用。结果脑缺血2h复流后1d缺血区周围及海马可见GAP-43mRNA表达,7d明显增多至高峰,14d开始下降,30d时则明显减少,CVB-D治疗组在上述区域各时间点较对照组显著增加。脑缺血再灌注7d后,治疗组较对照组大鼠脑水含量及梗死面积显著降低,受损脑组织神经元和血管壁的超微结构亦明显改善。结论CVB-D对RHRSP缺血性脑细胞损伤有一定保护作用,其促进轴突的再生可能与上调脑组织GAP-43mRNA表达有关。
Objective To observe the effect of CVB-D on the expression of GAP-43 mRNA in cerebral ischemia-reperfusion rats with stroke-induced renovascular hypertension (RHRSP) at different time points. And cell ultrastructure damage. Methods The bilateral renal arteries of SD rats were stenosed with a ring silver clip and made into RHRSP. The middle cerebral artery occlusion (MCAO) model was made by the method of thread plug. The expression of GAP-43mRNA, water content, percentage of infarction area, behavioral score and cell ultrastructure of CVB-D in rat brain at 1d, 7d, 14d and 30d after cerebral ischemia were observed by in situ hybridization Intervention of microstructure. Results The expression of GAP-43 mRNA in ischemic zone and hippocampus at 1 day after reperfusion was observed at 2 h after cerebral ischemia, and then increased to the peak at 7 d, decreased at 14 d and decreased significantly at 30 d. Compared with the control group Group increased significantly. After cerebral ischemia-reperfusion for 7 days, the brain water content and infarct size in the treatment group were significantly lower than those in the control group, and the ultrastructure of neurons and blood vessel wall in the damaged brain tissue was also significantly improved. Conclusions CVB-D can protect the ischemic brain cells of RHRSP to a certain extent, which may be related to the up-regulation of GAP-43mRNA expression in axon.