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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神经胶质原纤维酸性蛋白(GFAP)与神经粘蛋白(neurocan)表达的影响。方法100只SD大鼠随机分成随机分为空白组10只(不作任何处理的RHRSP)、假手术组10只(仅作手术创伤分离动脉,不结扎动脉)、CVB-D治疗组40只、生理盐水对照组40只。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。用免疫组化等方法观察CVB-D对脑缺血2h后再灌注1、7、14、30d不同时间点大鼠脑组织GFAP与neurocan表达。结果缺血2h再灌注后,治疗组脑缺血区周围GFAP阳性表达细胞呈现先递增后减少的趋势。与对照组相比,除第1天外,第7、14、30天差异都有显著性意义(P<0.05)。Neurocan在空白组、假手术组未见阳性细胞,缺血再灌注1d对照组出现neurocan阳性表达细胞,并且呈先递增后减少趋势。治疗组neurocan阳性表达细胞与对照组相比,除第1天外,第7、14、30天差异都有显著性意义(P<0.05)。结论CVB-D有促进RHRSP脑缺血损伤区神经功能的修复作用,可能与其下调神经抑制因子GFAP、neurocan的表达等机制密切相关。
Objective To observe the effect of CVB-D on proliferation and apoptosis of glial fibrillary acidic protein (GFAP) and neuromucin in rats with stroke-induced renovascular hypertension (RHRSP) (neurocan) expression. Methods 100 Sprague-Dawley rats were randomly divided into 10 rats (RHRSP without any treatment), 10 rats in the sham operation group (only for surgical traumatic dissection and non-ligated artery), 40 in CVB-D group Saline control group of 40. The bilateral renal arteries of SD rats were stenosed by a ring-shaped silver clip and made into RHRSP. One side of the middle cerebral artery occlusion (MCAO) model was made by the method of thread plug. The expression of GFAP and neurocan in CVB-D rats were observed by immunohistochemistry at different time points after reperfusion for 1, 2, 4, and 7 days. Results After reperfusion for 2 hours, the number of GFAP positive cells in the treatment group increased first and then decreased. Compared with the control group, except for the first day, there was a significant difference at the 7th, 14th, and 30th days (P <0.05). Neurocan in the blank group, sham operation group no positive cells, ischemic reperfusion 1d control group neurocan positive cells, and the first increase and then reduce the trend. Compared with the control group, the neurocan-positive cells in the treatment group had significant difference at the 7th, 14th and 30th days except the first day (P <0.05). Conclusions CVB-D can promote the repair of nerve function in ischemic area of RHRSP, which may be closely related to its mechanism of down-regulation of GFAP and neurocan.