西安交通大学学报（医学版）2017，Vol.38Issue(4)：522-528,7.DOI:10.7652/jdyxb201704011
P38MAPK通路对脑缺血后处理大鼠海马自噬的影响
Effect of P38MAPK pathway on autophagy in rat hippocampus following cerebral ischemic postcoditioning
摘要
Abstract
Objective To explore the mechanism of ischemic postconditioning in relieving cerebral ischemia reperfusion (IR) by regulating autophagy through P38MAPK pathway.Methods Cerebral ischemia reperfusion model was established by using modified Pulsinelli four-vessel occlusion (4-VO).Totally 128 male SD rats were divided into 4 groups randomly:control group (sham),cerebral ischemia reperfusion model group (CIR),cerebral ischemic postconditioning group (CIP),and cerebral ischemic postconditioning + P38MAPK inhibitor group (SB203580 group).Each group was subdivided into four time points:6 h,24 h,48 h,and 72 h.The morphological changes of the hippocampus CA1 area neurons at each time point and the number of surviving nerve cells were detected with HE staining.The expression of the hippocampus CA1 area phosphorylated P38MAPK and the autophagy-related genes of Beclin-1 and LC3-Ⅱ were detected with immunohistochemistry.The protein content of the hippocampus phosphorylated P38MAPK and autophagy-related genes of Beclin-1 and LC3-Ⅱ were detected with Western blotting.Results Compared with those in sham group,the damage of rats' hippocampal neuron structure and the survival rate of neurons at each time point decreased in CIR group,the expressions of p-P38MAPK,LC3-Ⅱ and Beclin-1 increased.Compared with those in CIR group,in CIP and SB203580 groups the structure of rats hippocampal neurons was improved,the survival rate of neurons increased,the expression of p-P38MAPK decreased and the expressions of LC3-Ⅱ and Beclin-1 increased at each time point.Compared with CIP group,SB203580 grouphad improved structure of rats' hippocampal neurons,increased survival rate of neurons,decreased expression of p-P38MAPK,and increased expressions of LC3-Ⅱ and Beclin-1 at each time point.Conclusion Cerebral ischemic postconditioning through inhibiting P38MAPK pathway can regulate autophagy and exert its nerve-protective effect.关键词
脑缺血再灌注/脑缺血后处理/P38MAPK/自噬/SB203580Key words
cerebral ischemia reperfusion/cerebral ischemic postconditioning/P38MAPK/autophagy/SB203580分类
医药卫生引用本文复制引用
刘瑶,赵雅宁,李建民,陈长香,刘宇..P38MAPK通路对脑缺血后处理大鼠海马自噬的影响[J].西安交通大学学报（医学版）,2017,38(4):522-528,7.基金项目
河北省重大医学课题(No.ZD2013093) （No.ZD2013093）
唐山市科技计划项目(No.14130220B)Supported by the Grand Medical Projects of Hebei Province (No.ZD2013093) and the Science and Technology Plan Projects of Tangshan (No.14130220B) （No.14130220B）
