本文關(guān)鍵詞： 腦 缺血再灌注損傷 缺血后適應(yīng) 自噬 哺乳動物雷帕霉素靶蛋白　出處：《中國病理生理雜志》2017年10期 　論文類型：期刊論文

【摘要】：目的:探討缺血后適應(yīng)對大鼠局灶性腦缺血再灌注所致自噬的影響。方法:取健康雄性SD大鼠30只,隨機分為假手術(shù)(sham)組、缺血再灌注(I/R)組、缺血后適應(yīng)(IPC)組,每組各10只。Sham組僅單純暴露右側(cè)頸總、頸內(nèi)和頸外動脈;I/R組采用Longa改良線栓法制備大鼠右側(cè)大腦中動脈缺血2 h、再灌注24 h模型;IPC組大鼠缺血2 h后,同側(cè)頸總動脈再通10 s/閉塞10 s,循環(huán)5次,然后全面恢復(fù)血流再灌注24 h。采用透射電鏡觀察腦細(xì)胞自噬情況;Western blot法測定各組大鼠腦組織中哺乳動物雷帕霉素靶蛋白(m TOR)、磷酸化m TOR(pm TOR)和微管相關(guān)蛋白輕鏈3(LC3)-Ⅱ的蛋白表達(dá)水平;TTC法檢測腦梗死面積;干濕稱重法測定腦組織含水量;HE染色觀察腦組織病理學(xué)變化。結(jié)果:IPC組m TOR、p-m TOR均顯著高于I/R組(P0.05),LC3-Ⅱ顯著低于I/R組(P0.01)。IPC組腦梗死面積、腦組織含水量均顯著低于I/R組(P0.01)。HE染色顯示,IPC組神經(jīng)元變性、壞死較I/R組明顯減輕。透射電鏡顯示IPC組神經(jīng)元損傷程度明顯減輕,自噬泡明顯減少。結(jié)論:IPC通過減少細(xì)胞內(nèi)自噬而減輕腦缺血再灌注損傷,可能與增強m TOR作用有關(guān)。
[Abstract]:Objective: to investigate the effect of ischemic adaptation on autophagy induced by focal cerebral ischemia reperfusion in rats. Methods: thirty healthy male SD rats were randomly divided into sham group. 10 rats in each group were exposed to the right total carotid artery, internal carotid artery and external carotid artery. In the I / R group, the right middle cerebral artery was ischemia for 2 h and reperfusion for 24 h. After ischemia for 2 hours in IPC group, the ipsilateral common carotid artery was recanalized for 10 s / 10 s, followed by 5 circulations, and then the blood flow was recovered completely for 24 h. The autophagy of brain cells was observed by transmission electron microscope (TEM). The mammalian rapamycin target protein (rapamycin) was determined by Western blot method. The protein expression level of phosphorylated m TOR(pm word) and microtubule-associated protein light chain 3C3F- 鈪，

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