本文選題：脊髓 + 缺血再灌注��； 參考：《南京醫(yī)科大學(xué)學(xué)報(bào)(自然科學(xué)版)》2015年11期

【摘要】：目的:探討缺血預(yù)處理保護(hù)脊髓神經(jīng)的具體機(jī)制。方法 :50只成年SD大鼠隨機(jī)分為假手術(shù)組(A組5只)、缺血再灌注組(B組20只)、缺血預(yù)處理組(C組5只)、缺血預(yù)處理+缺血再灌注組(D組20只)。A組動(dòng)物麻醉后僅切開腹腔后關(guān)腹;B組和D組采用左腎下方0.5 cm處腹主動(dòng)脈夾閉法夾閉0.5 h后松開,再灌注3、6、12、24 h,其中D組在缺血再灌注損傷前行缺血5 min、再灌注5 min缺血預(yù)處理,共3次;C組僅行3次缺血預(yù)處理。造模成功后,利用HE染色和免疫組化評(píng)估各組神經(jīng)元的存活率,透射電鏡觀察自噬活性,免疫組化和蛋白印跡分析自噬標(biāo)志物L(fēng)C3-Ⅱ和自噬相關(guān)蛋白Beclin-1的表達(dá)情況。結(jié)果:缺血再灌注組中,LC3-Ⅱ蛋白在再灌注3 h后顯著升高達(dá)到峰值后明顯下降,24 h后幾乎無表達(dá);Beclin-1蛋白于再灌注后3 h開始升高且在24 h達(dá)到峰值;再灌注24 h后實(shí)驗(yàn)動(dòng)物表現(xiàn)出明顯的脊髓損傷癥狀,脊髓神經(jīng)細(xì)胞存活率明顯降低。缺血預(yù)處理+缺血再灌注組中,LC3-Ⅱ蛋白表達(dá)從再灌注3 h開始升高并持續(xù)至再灌注24 h;Beclin-1蛋白在再灌注24 h后才開始升高;與缺血再灌注組相比,缺血預(yù)處理+缺血再灌注組脊髓神經(jīng)元死亡率明顯降低。結(jié)論:缺血預(yù)處理通過維持缺血再灌注后神經(jīng)細(xì)胞自噬水平并抑制自噬性細(xì)胞死亡從而保護(hù)脊髓神經(jīng)細(xì)胞。
[Abstract]:Objective: to investigate the protective mechanism of ischemic preconditioning on spinal cord nerve. Methods Fifty adult Sprague-Dawley rats were randomly divided into sham operation group (n = 5), ischemia reperfusion group (n = 20), ischemic preconditioning group (n = 5) and ischemic preconditioning group (n = 20). The abdominal aorta of group B and D were clamped 0.5 cm below the left kidney for 0.5 h and then released. The rats in group D received ischemic preconditioning for 5 min before ischemia and reperfusion for 5 min, and only 3 ischemic preconditioning were performed in group C for 3 times. The survival rate of neurons in each group was evaluated by HE staining and immunohistochemistry. The autophagy activity was observed by transmission electron microscope. The expression of autophagy marker LC3- 鈪，

本文編號(hào)：1852476