人参皂甙Rg1对脑缺血再灌注大鼠pJNK表达影响.docVIP

人参皂甙Rg1对脑缺血再灌注大鼠pJNK表达影响 　【摘要】 　　目的 探讨人参皂甙Rg1对脑缺血再灌注大鼠脑组织c-jun N-末端激酶（pJNK）表达的影响及其意义。方法将大鼠随机分为假手术组、单纯缺血再灌注组、人参皂甙Rg1 10、20、40 mg/kg组、尼莫地平1 mg/kg组，采用大脑中动脉闭塞法建立脑缺血再灌注模型,应用免疫组织化学方法检测脑组织缺血再灌注4h后pJNK的表达。 结果 人参皂甙Rg1各剂量组大鼠脑组织pJNK表达阳性率分别为(23.89±6.77), (15.19±4.59), (9.15±4.77)，均低于单纯缺血再灌注组 (27.15±8.46)。结论 人参皂甙Rg1防治大鼠脑缺血再灌注损伤的机制可能与抑制脑组织pJNK表达有关，且以高剂量效果较好。 【关键词】 人参皂甙Rg1 脑缺血再灌注 pJNK 大鼠 　　Abstract: Objective To discuss the effects of Ginsenoside Rg1 on the expressions of JNK in the rats brain tissue after focal cerebral ischemia-reperfusion and its significance. Methods Rats were divided into the sham-operative group, Model group, Ginsenoside Rg1 groups of 10 mg/kg, 20 mg/kg, 40mg/kg, and Nimodipine group of 1 mg/kg at random. The method of middle cerebral artery occlusion (MCAO) in rats was adopted to establish the model of cerebral ischemia-reperfusion, and then the expressions of JNK after cerebral ischemia-reperfusion 6 h was tested based on the chemical method in immunity tissue. Results The positive rate of expression of rats brain tissue in each of the Ginsenoside Rg1 groups is (23.89±6.77), (15.19±4.59), (9.15±4.77) respectively. Conclusions The results showed that the mechanism of Ginsenoside Rg1 to protect the brain cells from damage after cerebral ischemia-reperfusion injury may be associated with JNK expression to inhibit brain tissue, and it was more effective when Ginsenoside Rg1 was in high-dose． 　　Key words:Ginsenoside Rg1; cerebral ischemia-reperfusion; JNK；rat 　　研究表明，人参皂甙Rg1能通过抑制细胞凋亡对脑缺血再灌注损伤发挥保护作用，但其抗凋亡的机制还不十分清楚［1］。丝裂原蛋白激酶信号通路(mitogen activated protein kinases，MAPKs)是脑缺血再灌注损伤中主要的信号通路，它包括5个亚家族，其中c-Jun氨基末端激酶(c-Jun N-terminal kinases，JNKs)亚家族主要参与细胞凋亡的调控。本实验拟采用免疫组织化学方法检测脑缺血再灌注后大鼠海马CA1区神经元pJNK的表达，并观察人参皂甙Rg1对pJNK蛋白表达的影响，以明确人参皂甙Rg1是否通过JNK信号通路来抑制脑缺血再灌注后的神经元凋亡。 　　1 材料与方法 　　1.1 实验动物分组与给药方法 　　Sprage-Dawl大鼠，雄性（以排除雌激素影响），体重为250～300 g，随机分为6组：①假手术组；②单纯缺血再灌注组；③～⑤人参皂甙Rg1给药组（10、20、40 mg/kg）；尼莫地平药物对照组（1 mg/kg）；每组5只大鼠。③～⑥组分别于术前5 d至取材当日腹腔注射人参皂甙Rg1、尼莫地平，其余