本文選題：蛛網(wǎng)膜下腔出血 + 早期腦損傷��； 參考：《西安交通大學(xué)學(xué)報(bào)(醫(yī)學(xué)版)》2017年01期

【摘要】：目的探討ERK信號通路特異性抑制劑U0126對蛛網(wǎng)膜下腔出血(SAH)對早期腦損傷及海馬區(qū)神經(jīng)細(xì)胞自噬的作用。方法成年雄性SD大鼠48只,隨機(jī)數(shù)字表法分為對照組、SAH組、DMSO+SAH(二甲基亞砜)組、U0126+SAH組(ERK信號通路特異性抑制劑),共4組,每組各12只。采用血管內(nèi)穿刺法(PIC)法制作SAH模型,分別于造模前30min經(jīng)尾靜脈注射等量的生理鹽水、DMSO、U0126溶液0.5mL/只,于24h處死。干濕重法測量腦組織水含量,HE染色觀察海馬CA1區(qū)神經(jīng)細(xì)胞形態(tài)結(jié)構(gòu)變化;免疫組化及Western bloting檢測海馬區(qū)ERK及Beclin-1和LC3-Ⅱ表達(dá)水平的變化。結(jié)果與Sham組比較,SAH模型組腦組織含水量明顯增加,大鼠海馬CA1區(qū)神經(jīng)元數(shù)量明顯減少(P0.05),ERK及自噬相關(guān)因子Beclin-1和LC3-Ⅱ的表達(dá)明顯高于對照組(P0.05);與SAH模型組比較,U0126組腦組織含水量明顯增多,海馬CA1區(qū)神經(jīng)元數(shù)量明顯較SAH組減少(P0.05),ERK信號信號通路被抑制,相應(yīng)自噬相關(guān)因子Beclin-1和LC3-Ⅱ的表達(dá)降低(P0.05)。結(jié)論ERK信號通路抑制劑U0126可以抑制神經(jīng)細(xì)胞自噬,加重SAH的早期腦損傷。
[Abstract]:Objective to investigate the effects of ERK signal pathway specific inhibitor U0126 on early brain injury and hippocampal neuronal autophagy in patients with subarachnoid hemorrhage. Methods Forty-eight adult male Sprague-Dawley rats were randomly divided into 4 groups (12 rats in each group) with DMSO SAH (dimethyl sulfoxide) group and U0126 SAH group. The SAH model was made by intravascular puncture method. 30min was injected into the tail vein with the same amount of 0.5mL/ solution DMSOSOU0126, and was killed at 24 hours. The changes of neuronal morphology and structure of hippocampal CA1 were observed by HE staining, and the changes of ERK, Beclin-1 and LC3- 鈪，

本文編號：1950435