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目的观察补阳还五汤对局灶性脑缺血大鼠神经导向因子Slit2及其受体Robo1蛋白表达的影响,探讨其对脑缺血神经保护作用机制。方法采用改良大脑中动脉线栓法建立脑缺血模型(MCAO),90只SD大鼠按照随机数字表法分成假手术组、模型组、补阳还五汤组共3组,每组30只,每组分别于脑缺血后3天、7天、14天检测相关指标,采用修订神经功能评分(m NSS)观察大鼠神经功能恢复情况,采用免疫组化、Western-blot检测各组大鼠脑缺血后不同时间点Slit2,Robo1蛋白的表达。结果各个时间点MCAO模型大鼠动物都出现了明显的神经功能缺损,补阳还五汤组可显著缓解这些神经症状,降低行为学评分。免疫组化及Western-blot检测结果显示模型组Slit2,Robo1蛋白在第3,7天表达增多,与同时间段假手术组比,差异有统计学意义(P<0.01,P<0.05),随后表达逐渐下降,补阳还五汤组能上调Slit2表达,第3天上调最明显(P<0.05),同时上调Robo1表达,其中在7天上调最明显,与同时段模型组比较差异具有统计学意义(P<0.05)。结论补阳还五汤能调控脑缺血后大鼠Slit2,Robo1蛋白的表达,促进神经功能恢复,这可能是其治疗脑缺血的机制之一。
Objective To observe the effect of Buyang Huanwu Decoction on the expression of neurotransmitter Slit2 and its receptor Robo1 in focal cerebral ischemia rats and to explore its neuroprotective mechanism. Methods Cerebral ischemia model (MCAO) was established by modified middle cerebral artery occlusion (MCAO). 90 SD rats were randomly divided into sham operation group, model group and Buyang Huanwu Decoction group with 30 rats in each group , Respectively. The indexes in each group were detected at 3 days, 7 days and 14 days after cerebral ischemia. The neurological function recovery was observed by m NSS. Immunohistochemistry and Western-blot were used to detect The expression of Slit2 and Robo1 protein at different time points after cerebral ischemia in rats. Results At each time point, obvious neurological impairment occurred in the MCAO model rats. BYHWD group could relieve these neurological symptoms and reduce the behavioral score. The results of immunohistochemistry and Western-blot showed that the expressions of Slit2 and Robo1 increased on the 3rd and 7th day in the model group compared with those in the sham operation group at the same time (P <0.01, P <0.05) The expression of Slit2 was up-regulated in Buyang Huanwu Decoction group, the up-regulation was the highest on the 3rd day (P <0.05), and the expression of Robo1 was up-regulated at the 7th day Significance (P <0.05). Conclusion Buyang Huanwu Decoction can regulate the expression of Slit2 and Robo1 protein in rats after cerebral ischemia and promote the recovery of nerve function, which may be one of the mechanisms of its treatment of cerebral ischemia.