P38MAPK通路对脑缺血后处理大鼠海马自噬的影响

发布时间：2018-04-17 22:16

  本文选题：脑缺血再灌注 + 脑缺血后处理　； 参考：《西安交通大学学报(医学版)》2017年04期

【摘要】：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+P38MAPK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。
[Abstract]:Objective to investigate the mechanism of P38MAPK pathway regulating autophagy to reduce cerebral ischemia-reperfusion injury after cerebral ischemia.Methods the model of cerebral ischemia was established by modified Pulsinelli four-vessel occlusion (4-VOO) method.128 male Sprague-Dawley rats were randomly divided into four groups: sham-operated group, cerebral ischemia-reperfusion model group, cerebral ischemia post-treatment group, P38MAPK inhibitor group, SB203580 group. Each group was divided into 4 groups for 72 hours.The morphology of neurons and the number of viable neurons in hippocampal CA1 were observed by HE staining.The expression of phosphorylated P38MAPK in hippocampal CA1 and the expression of autophagy associated gene Beclin-1hLC3- 鈪，

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