黄芪甲苷通过激活JNK/p38 MAPK信号通路对急性脑梗死模型大鼠神经功能的影响  

Effect of astragaloside IV on neurological function of rats with acute cerebral infarction by activating the JNK/p38 MAPK signaling pathway

作　　者：王仙丽[1] 刘艳[1] 李婷 陈春艳[1] WANG Xianli;LIU Yan;LI Ting(Department of Neurology,Bayannur Hospital,Inner Mongolia,Bayannur 015000,China)

机构地区：[1]巴彦淖尔市医院神经内科,内蒙古自治区015000

出　　处：《河北医药》2024年第6期816-820,共5页Hebei Medical Journal

基　　金：内蒙古自治区卫生健康科技计划项目(编号:202201625)。

摘　　要：目的分析黄芪甲苷通过激活c-Jun氨基末端激酶(JNK)/p38丝裂原活化蛋白激酶(p38 MAPK)信号通路对急性脑梗死模型大鼠神经功能的影响。方法选取50只健康SPF级SD大鼠,10只作为对照组,其余40只建立急性脑梗死模型,其中30只大鼠建模成功,将30只大鼠随机分为模型组、药物对照组、黄芪甲苷组,每组10只对建模成功的大鼠进行给药处理,对照组、模型组大鼠采用0.9%氯化钠溶液灌胃,药物对照组给予20 mg/kg阿托伐他汀灌服,黄芪甲苷组给予70 mg/kg黄芪甲苷应用液灌服,均灌胃12周。观察4组大鼠病理组织学、神经功能[神经元特异性烯醇化酶(NSE)、星形胶质源性蛋白(S100β)]、氧化应激指标[超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、丙二醛(MDA)、活性氧(ROS)]、炎性因子[肿瘤坏死因子α(TNF-α)、白介素-1β(IL-1β)、C反应蛋白(CRP)]、JNK/p38 MAPK通路相关mRNA表达量、JNK/p38 MAPK通路。结果与对照组比较,模型组、药物对照组、黄芪甲苷组SOD、CAT降低,NSE、S100β、MDA、ROS、TNF-α、IL-1β、CRP、JNK、p38 MAPK mRNA、JNK、p38 MAPK升高(P<0.05);与模型组比较,药物对照组、黄芪甲苷组SOD、CTA升高,NSE、S100β、MDA、ROS、TNF-α、IL-1β、CRP、JNK、p38 MAPK mRNA、JNK、p38 MAPK降低,(P<0.05);与药物对照组比较,黄芪甲苷组SOD、CTA升高,NSE、S100β、MDA、ROS、TNF-α、IL-1β、CRP、JNK、p38 MAPK mRNA、JNK、p38 MAPK降低(P<0.05)。结论采用黄芪甲苷对急性脑梗死模型大鼠干预,可改善大鼠氧化应激指标,降低炎性反应,使大鼠神经功能得到改善,其作用机制可能与调控JNK/p38 MAPK信号通路有关。Objective To analyze the effect of astragaloside IV on neurological function of rats with acute cerebral infarction via activating the c-Jun amino terminal kinase(JNK)/p38 mitogen-activated protein kinase(p38 MAPK)signaling pathway.Methods Fifty healthy Sprague-Dawley(SD)rats in the specific pathogen free(SPF)level were selected.Ten were randomly selected as control group without specific treatment,and the remaining 40 rats were used to establish an acute cerebral infarction model.A total of 30 rats were successfully prepared for the modeling of acute cerebral infarction,and they were randomly divided into model group,drug control group and astragaloside group,with 10 rats per group.Rats in the control group and model group were given 0.9% sodium chloride solution by gavage.Gavage of 20mg/kg atorvastatin and 70mg/kg astragaloside Ⅳ solution was performed for 12 weeks in rats of drug control group and astragaloside group,respectively.Pathological changes,neurological function(neuron-specific enolase[NSE],S100 calcium-binding protein B[S100B]),oxidative stress(superoxide dismutase[SOD],catalase[CAT],malondialdehyde[MDA],reactive oxygen species[ROS]),inflammatory factors[tumor necrosis factorα[TNF-α],interleukin-1β[IL-1β],C-reactive protein[CRP]),mRNA level and protein levels of JNK and p38 MAPK were compared.Results Compared with those of the control group,rats in the model group,drug control group and astragaloside group presented significantly lower SOD and CAT,and significantly higher NSE,S100β,MDA,ROS,TNF-α,IL-1β,CRP,JNK,mRNA level of p38 MAPK and protein levels of JNK and p38 MAPK(P<0.05).Compared with those of model group,rats in the drug control group and astragaloside group presented significantly higher SOD and CAT,and significantly lower NSE,S100β,MDA,ROS,TNF-α,IL-1β,CRP,JNK,mRNA level of p38 MAPK and protein levels of JNK and p38 MAPK(P<0.05).Compared with those of drug control group,rats in the astragaloside group presented significantly higher SOD and CAT,and significantly lower NSE,S100β,

关 键 词：急性脑梗死 C-JUN氨基末端激酶 P38丝裂原活化蛋白激酶 黄芪甲苷 神经功能 

分 类 号：R743.3[医药卫生—神经病学与精神病学]