P38MAPK通路对脑缺血后处理大鼠海马自噬的影响

P38MAPK通路对脑缺血后处理大鼠海马自噬的影响
刘瑶;赵雅宁;李建民;陈长香;刘宇
【期刊名称】《西安交通大学学报（医学版）》
【年(卷),期】2017(38)4
【摘要】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 pared 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 pared 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.%目的探讨脑缺血后处理通过P38MAPK通路调控自噬减轻脑缺血再灌注损伤的机制.方法采用改良的Pulsinelli四血管闭塞(4-VO)法制
作脑缺血模型,随机将128只雄性SD大鼠平均分为4组:假手术组(Sham组)、脑
缺血再灌注模型组(CIR组)、脑缺血后处理组(CIP组)、脑缺血后处理+P38 MAPK 抑制剂组(SB203580组),每组再分为6、24、48、72h四个时间点.应用HE染色
观察海马CA1区各时间点神经元的形态及存活神经细胞数量;免疫组织化学染色法测定海马CA1区磷酸化P38MAPK和自噬相关基因Beclin-1、LC3-Ⅱ的表
达;Western blotting法检测海马组织磷酸化P38MAPK和自噬相关基因Beclin-1、LC3-Ⅱ的蛋白含量.结果与Sham组比较,CIR组大鼠海马CA1区神经元结构破坏,各时间点存活神经元数量下降,磷酸化P38MAPK表达增加,LC3-Ⅱ、Beclin-1表
达增加;与CIR组比较,CIP组和SB203580组神经元结构改善,各时间点存活神经元数量增加,磷酸化P38MAPK各时间点表达水平下降,LC3-Ⅱ、Beclin-1表达增加;
与CIP组比较,SB203580组海马CA1区神经元结构明显改善,各时间点存活神经元
数量增加,磷酸化P38MAPK各时间点表达水平下降,LC3-Ⅱ、Beclin-1表达增加.结论脑缺血后处理可能通过抑制P38MAPK通路调控自噬,发挥其神经保护作用.【总页数】7页(P522-528)
【作者】刘瑶;赵雅宁;李建民;陈长香;刘宇
【作者单位】华北理工大学护理与康复学院,河北唐山063000;华北理工大学护理与康复学院,河北唐山063000;华北理工大学附属医院,河北唐山063000;华北理工大学护理与康复学院,河北唐山063000;华北理工大学护理与康复学院,河北唐山063000
【正文语种】中文
【中图分类】R743.3
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