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目的:探讨人参皂苷Rg1(Ginsenoside Rg1,Rg1)抑制氯化锂-匹罗卡品联合诱导的癫痫大鼠模型大脑胼胝体区小胶质细胞(microglia,MG)的激活和炎性因子的表达作用,为临床应用Rg1治疗癫痫提供理论依据。方法:80只健康雄性SD大鼠随机分为4组:即空白对照组、模型组、Rg1预治疗组、卡马西平(carbamazepine,CBZ)预治疗组,每组20只;采用氯化锂-匹罗卡品腹腔注射制备癫痫大鼠模型,治疗组提前进行药物预处理,模型组给予相同剂量的生理盐水,记录行为学发作情况,注射匹罗卡品后2 h给予安定终止,3 d后取材;免疫荧光组织化学染色和Western Blot检测大脑胼胝体区精氨酸酶1(arginase-1,Arg-1)、诱导型一氧化氮合酶(induced nitric oxide synthase,iN OS)和白介素1β(interleukin-1β,IL-1β)的蛋白表达变化。结果:与模型组相比,Rg1预治疗组明显缩短癫痫大鼠的大发作时间;模型组与空白对照组比较,大脑胼胝体区MG明显激活,胞体变圆,突起减少,呈“M1型”阿米巴样状态;Rg1预治疗组较模型组相比,MG的激活明显降低,Arg-1蛋白的表达明显上调,iN OS和IL-1β等炎性因子的表达显著下调。结论:Rg1增加癫痫大鼠大脑胼胝体区Arg-1蛋白的表达,降低iN OS和IL-1β等炎性因子的表达,抑制MG的激活和极化,减轻炎症因子的表达,缩短癫痫大鼠大发作时间。
Objective: To investigate the effect of ginsenoside Rg1 (Rg1) on the activation of microglia (MG) and the expression of inflammatory cytokines in the brain of the epileptic rats induced by lithium chloride - pilocarpine, Provide a theoretical basis for the clinical application of Rg1 in the treatment of epilepsy. Methods: Eighty healthy male SD rats were randomly divided into 4 groups: control group, model group, Rg1 pretreatment group and carbamazepine (CBZ) pretreatment group, with 20 rats in each group. Lithium chloride - Pilocarpine was intraperitoneally injected to prepare the epilepsy rat model. The treatment group was given the drug pretreatment in advance. The model group was given the same dose of saline, and the behavioral attack was recorded. After 2 h injection of pilocarpine, diazepam was stopped. After 3 d The expression of arginase-1 (Arg-1), induced nitric oxide synthase (iNOS) and interleukin-1β (IL-1β) in the brain were detected by immunofluorescence staining and Western Blot. -1β, IL-1β) protein expression changes. Results: Compared with the model group, the Rg1 pretreatment group significantly shortened the onset time of epilepsy rats. Compared with the blank control group, MG in the model group was significantly activated in the corpus callosum area, Compared with model group, the activation of MG in Rg1 pretreatment group was significantly decreased, the expression of Arg-1 protein was significantly increased, and the expression of inflammatory factors such as iNOS and IL-1β were significantly down-regulated. Conclusion: Rg1 can increase the expression of Arg-1 in the corpus callosum of epileptic rats, decrease the expression of inflammatory factors such as iNOS and IL-1β, inhibit the activation and polarization of MG, decrease the expression of inflammatory cytokines and shorten the expression of Arg- Attack time.