中文摘要：

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。

英文摘要：

Objective： In order to provide theoretical support of ginsenoside Rg1（ Rg1） in treatment of epilepsy in clinic,we explored the role of Rg1 in attenuating activation of microglia（ MG） and expression of inflammatory factors in the corpus callosum region on epileptic rats model induced by lithium chloride-pilocarpine. Methods： Eighty healthy male rats were randomly divided into four groups： control group,model group,Rg1 pretreatment group and carbamaz-epine（ CBZ） pretreatment group,each group has 20 rats. Epileptic model was established by lithium chloride-pilocarpine intraperitoneal injection; The pretreatment groups were given Rg1 or CBZ in advance,and same dosage of normal saline was given to model group. Behavior changes was recorded. The seizure was terminated with valium（ diazepam） 2h after given pilocarpine,the brain was fetched after 3 d. The morphology and the expression change of arginase-1（ Arg-1）,induced nitric oxide synthase（ iN OS）,interleukin-1β（ IL-1β） in the corpus callosum region were detected by immunofluorescence staining and Western Blot. Results： The total seizure time in Rg1 pretreatment group was less than control group. Comparing to control group,microglia cells in the corpus callosum region in the modal group were significantly activated,the processes was shorten,volume got bigger,most of them seemed as amoebocyte. Meanwhile,the expression of Arg-1 was obviously upregulated,iN OS and IL-1β were evidently downregulated in the model group,Rg1 pretreatment group attenuate the activation of microglia cells,simultaneously,the expression of Arg-1 was significantly increased,while iN OS and IL-1β were markedly decreased. Conclusion： Rg1 up-regulate the Arg-1 protein,and down-regulate the expression of iN OS and IL-1β,depress the activation and polarization of microglia,inhibit the expression of inflammatory reaction,short the seizure time in epileptic rat.