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自由基导致的神经细胞损伤是中风发病机理之一。多项体外和体内研究证明,通过干预自由基在局部缺血部位导致的细胞凋亡,抗氧化剂可起到神经保护作用,而具有抗氧化功效的自然产品无疑是一种极有潜力的治疗中风的候选药物。本研究的目的是评估脑必通(Braintone)在Wistar大鼠大脑中动脉梗死模型(MCAO)的治疗作用。与对照组相比,脑必通治疗组大鼠促凋亡基因(AT2受体,FAS,BAX和BCL-XS)的表达量显著地减少(分别是0.4-,0.72-,0.76-,0.32倍,P<0.05)。免疫组化结果显示这些基因所对应的蛋白质表达量也大量减少。TUNEL的观察结果进一步验证了脑必通的抗凋亡作用,从而证明脑必通作为一种抗氧化药物,对中风的治疗的确具有一定的潜在功效。
Free radical-induced neuronal damage is one of the pathogenesis of stroke. A number of in vitro and in vivo studies have demonstrated that antioxidants can play a neuroprotective role by interfering with apoptosis induced by free radicals in ischemic sites, and natural products with antioxidant properties are undoubtedly a potential therapeutic stroke. Drug candidates. The purpose of this study was to evaluate the therapeutic effect of Braintone on the MCAO model in Wistar rats. Compared with the control group, the expression levels of the pro-apoptotic genes (AT2 receptor, FAS, BAX, and BCL-XS) in the brain-pass-treatment group were significantly reduced (0.4-, 0.72-, 0.76-, and 0.32-fold, respectively). P<0.05). The results of immunohistochemistry showed that the expression of the proteins corresponding to these genes was also greatly reduced. The observation of TUNEL further validated the anti-apoptotic effect of Nabitong, thus demonstrating that Brain Bitong, as an antioxidant drug, does have some potential efficacy in the treatment of stroke.