Effect of astragaloside Ⅳ on neurological function of rats with acute cerebral infarction by activating the JNK/p38 MAPK signaling pathway
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 factor α[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,MDA,ROS,TNF-α,IL-1β,CRP,JNK,mRNA level of p38 MAPK and protein levels of JNK and p38 MAPK(P<0.05).Conclusion Astragaloside Ⅳ treatment significantly alleviates oxidative stress and inflammatory response and improves neurological function in rats with acute cerebral infarction by activating the JNK/p38 MAPK signaling pathway.
acute cerebral infarctionC-Jun amino terminal kinaseP38 mitogen activated protein kinaseastragaloside Ⅳneurological function
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