本文選題：腦缺血再灌注 + 腦缺血后處理　； 參考：《西安交通大學(xué)學(xué)報(醫(yī)學(xué)版)》2017年04期

【摘要】：目的探討腦缺血后處理通過P38MAPK通路調(diào)控自噬減輕腦缺血再灌注損傷的機(jī)制。方法采用改良的Pulsinelli四血管閉塞(4-VO)法制作腦缺血模型,隨機(jī)將128只雄性SD大鼠平均分為4組:假手術(shù)組(Sham組)、腦缺血再灌注模型組(CIR組)、腦缺血后處理組(CIP組)、腦缺血后處理+P38MAPK抑制劑組(SB203580組),每組再分為6、24、48、72h四個時間點。應(yīng)用HE染色觀察海馬CA1區(qū)各時間點神經(jīng)元的形態(tài)及存活神經(jīng)細(xì)胞數(shù)量;免疫組織化學(xué)染色法測定海馬CA1區(qū)磷酸化P38MAPK和自噬相關(guān)基因Beclin-1、LC3-Ⅱ的表達(dá);Western blotting法檢測海馬組織磷酸化P38MAPK和自噬相關(guān)基因Beclin-1、LC3-Ⅱ的蛋白含量。結(jié)果與Sham組比較,CIR組大鼠海馬CA1區(qū)神經(jīng)元結(jié)構(gòu)破壞,各時間點存活神經(jīng)元數(shù)量下降,磷酸化P38MAPK表達(dá)增加,LC3-Ⅱ、Beclin-1表達(dá)增加;與CIR組比較,CIP組和SB203580組神經(jīng)元結(jié)構(gòu)改善,各時間點存活神經(jīng)元數(shù)量增加,磷酸化P38MAPK各時間點表達(dá)水平下降,LC3-Ⅱ、Beclin-1表達(dá)增加;與CIP組比較,SB203580組海馬CA1區(qū)神經(jīng)元結(jié)構(gòu)明顯改善,各時間點存活神經(jīng)元數(shù)量增加,磷酸化P38MAPK各時間點表達(dá)水平下降,LC3-Ⅱ、Beclin-1表達(dá)增加。結(jié)論腦缺血后處理可能通過抑制P38MAPK通路調(diào)控自噬,發(fā)揮其神經(jīng)保護(hù)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，

本文編號：1765532