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目的观察选择性诱导型一氧化氮合酶抑制剂氨基胍(AG)对局灶性脑缺血诱导大鼠脑神经元凋亡的影响,探讨AG对脑缺血大鼠脑神经元的保护作用及其机制。方法健康雄性SD大鼠54只,体重250-300 g,随机分为3组:假手术组(SH组)、缺血组(IS组)、AG治疗组(AG组),每组18只。每组按给药时机分为3个亚组:缺血2 h组、缺血6 h组、缺血12 h组,每亚组6只。IS、AG组采用插线法制备大鼠大脑中动脉阻断模型。AG组每次腹腔注射AG 100 mg/kg,每日2次,连续3 d。IS 组给予等量的生理盐水。治疗后大鼠断头取脑,采用流式细胞仪测定脑组织神经元凋亡率、Bcl-2蛋白、Bax蛋白表达及Bcl-2蛋白与Bax蛋白比值(Bcl-2/Bax)。结果与SH组比较,IS、AG组各亚组神经元凋亡率及Bax蛋白表达升高,AG组各亚组Bcl-2蛋白表达升高,IS、AG组各亚组Bcl-2/Bax降低(P <0.01);与IS组比较,AG组各亚组神经元凋亡率降低,AG组各亚组Bcl-2蛋白表达及Bcl-2/Bax升高,AG组Bax蛋白表达降低(P<0.05或0.01)。结论AG通过增加Bcl-2蛋白表达,降低Bax蛋白表达,调节Bcl-2/Bax平衡,对脑缺血大鼠脑神经元产生一定程度的保护作用。
Objective To observe the effect of selective inducible nitric oxide synthase inhibitor aminoguanidine (AG) on neuronal apoptosis induced by focal cerebral ischemia in rats, and to explore the protective effect of AG on neurons in cerebral ischemia rats And its mechanism. Methods Fifty-four healthy male Sprague-Dawley rats weighing 250-300 g were randomly divided into three groups: sham operation group (SH group), ischemia group (IS group) and AG treatment group (AG group), with 18 rats in each group. Each group according to the timing of administration is divided into three subgroups: ischemic 2 h group, ischemia 6 h group, ischemia 12 h group, 6 per subgroup. IS, AG group were inserted into the middle cerebral artery occlusion rat model. The AG group was given intraperitoneal injection of AG 100 mg / kg twice a day for 3 days. IS group given the same amount of saline. After treatment, the rats were decapitated and the brain apoptosis rate, Bcl-2 protein and Bax protein expression and Bcl-2 / Bax protein ratio were determined by flow cytometry. Results Compared with SH group, the apoptosis rate of neurons and the expression of Bax protein increased in all subgroups of IS and AG groups. The expression of Bcl-2 protein in subgroups of AG and AG increased significantly (P <0.01). Compared with IS group, the apoptosis rate of neurons in AG subgroup decreased, the expression of Bcl-2 protein and Bcl-2 / Bax in AG subgroup increased, P <0.05 or 0.01). Conclusion AG can protect neurons from cerebral ischemia in a certain degree by increasing Bcl-2 protein expression, decreasing Bax protein expression and regulating Bcl-2 / Bax balance.