本文選題：自噬 + 凋亡��； 參考：《河北聯(lián)合大學(xué)》2014年碩士論文

【摘要】：目的研究腦缺血預(yù)處理對(duì)大鼠局灶性腦缺血再灌注后自噬及凋亡的影響。 方法采用線(xiàn)栓法建立大鼠右側(cè)大腦中動(dòng)脈缺血預(yù)處理和缺血再灌注模型，將實(shí)驗(yàn)動(dòng)物隨機(jī)分為3組：假手術(shù)組、缺血再灌注組及缺血預(yù)處理組，各組按照再灌注后2h、6h、12h、24h、3d、5d分為6個(gè)亞組，各亞組大鼠在規(guī)定時(shí)間點(diǎn)行神經(jīng)功能障礙評(píng)分觀(guān)察神經(jīng)功能缺損情況，，TTC染色觀(guān)察腦梗死體積，HE染色觀(guān)察腦組織病理形態(tài)，免疫組織化學(xué)染色觀(guān)察自噬及凋亡相關(guān)蛋白Beclin-l、LC3-II、Bcl-2、Caspase-3表達(dá)變化，透射電子顯微鏡觀(guān)察神經(jīng)細(xì)胞中自噬及凋亡形態(tài)結(jié)構(gòu)變化。 結(jié)果1與假手術(shù)組大鼠相比，缺血再灌注組及缺血預(yù)處理組大鼠均可見(jiàn)不同程度神經(jīng)功能缺損、缺血側(cè)大腦半球梗死及梗死區(qū)神經(jīng)細(xì)胞損傷。與缺血再灌注組大鼠相比，缺血預(yù)處理組大鼠神經(jīng)功能障礙評(píng)分明顯減低（P0.05），缺血側(cè)大腦半球梗死體積明顯縮�。≒0.05），梗死區(qū)神經(jīng)細(xì)胞損傷明顯減輕。2與假手術(shù)組大鼠相比，缺血再灌注組及缺血預(yù)處理組大鼠再灌注后各時(shí)間點(diǎn)Beclin-l和LC3-II表達(dá)不同程度增多。與缺血再灌注組大鼠相比，缺血預(yù)處理組大鼠再灌注后各時(shí)間點(diǎn)Beclin-l和LC3-II表達(dá)不同程度減少（P0.05）。3與假手術(shù)組大鼠相比，缺血再灌注組及缺血預(yù)處理組大鼠再灌注后各時(shí)間點(diǎn)Bcl-2和Caspase-3表達(dá)不同程度增多。與缺血再灌注組大鼠相比，缺血預(yù)處理組大鼠再灌注后各時(shí)間點(diǎn)Bcl-2表達(dá)不同程度增多（P0.05），Caspase-3表達(dá)不同程度減少（P0.05）。4假手術(shù)組大鼠神經(jīng)細(xì)胞未見(jiàn)自噬及凋亡形態(tài)結(jié)構(gòu)。缺血再灌注后2h可見(jiàn)少量自噬溶酶體，凋亡仍不明顯；缺血再灌注后6h自噬溶酶體數(shù)量增多，可見(jiàn)輕度細(xì)胞凋亡改變；缺血再灌注后12~24h自噬溶酶體數(shù)量增多，細(xì)胞凋亡改變程度增加，表現(xiàn)為核染色質(zhì)塊狀邊集，核形態(tài)不規(guī)則等，持續(xù)到3d；缺血再灌注后5d仍可見(jiàn)自噬及凋亡形態(tài)結(jié)構(gòu)。缺血預(yù)處理組大鼠與缺血再灌注組大鼠相比，神經(jīng)細(xì)胞自噬及凋亡發(fā)生程度減低。 結(jié)論1腦缺血再灌注可損傷神經(jīng)細(xì)胞，使細(xì)胞發(fā)生自噬及凋亡，表現(xiàn)為神經(jīng)功能缺損，缺血側(cè)大腦半球梗死及梗死區(qū)神經(jīng)細(xì)胞損傷，自噬及凋亡相關(guān)蛋白Beclin-l、LC3-II、Bcl-2和Caspase-3表達(dá)顯著增加，神經(jīng)細(xì)胞自噬溶酶體數(shù)量增多，并出現(xiàn)明顯的細(xì)胞凋亡改變。2腦缺血預(yù)處理對(duì)神經(jīng)細(xì)胞具有保護(hù)作用，使細(xì)胞自噬及凋亡發(fā)生程度減低，表現(xiàn)為減少神經(jīng)功能缺損，縮小缺血側(cè)大腦半球梗死體積及減輕梗死區(qū)神經(jīng)細(xì)胞損傷，自噬及凋亡相關(guān)蛋白Beclin-l、LC3-II和Caspase-3表達(dá)明顯減少，Bcl-2表達(dá)明顯增多，神經(jīng)細(xì)胞自噬溶酶體數(shù)量減少，而且細(xì)胞凋亡改變程度減低。
[Abstract]:Objective to study the effect of ischemic preconditioning on autophagy and apoptosis after focal cerebral ischemia reperfusion in rats.
Methods to establish the rat middle cerebral artery ischemia preconditioning and ischemia reperfusion model by using suture method, the experimental animal were randomly divided into 3 groups: sham operation group, ischemia reperfusion group and ischemic preconditioning group, each group in 2h after reperfusion, 6h, 12h, 24h, 3D, 5D is divided into 6 sub groups, each sub group of rats at the specified time point for observation of neurological dysfunction score of neurological function, infarct volume was observed with TTC staining, to observe the brain tissue pathological HE staining, observe the autophagy and apoptosis related protein Beclin-l, immunohistochemistry staining of LC3-II, Bcl-2, Caspase-3 expression changes were observed by transmission electron microscopy, nerve cell autophagy apoptosis and morphological changes.
Results 1 rats compared with sham operation group, ischemia reperfusion group and ischemic preconditioning group rats showed different degrees of neurological defects, ischemic cerebral hemisphere infarction and infarction area of nerve cell injury. Compared with ischemia reperfusion rats, ischemic preconditioning group rats decreased obviously (P0.05 nerve function disorder), ischemic cerebral hemisphere infarction volume was significantly reduced (P0.05), nerve cell injury infarct area significantly reduced.2 than those of sham operation group rats, ischemia reperfusion group and ischemic preconditioning group after reperfusion in rats at different time points of Beclin-l and LC3-II expression increased at different degrees. Compared with the ischemia-reperfusion group rats. Ischemic preconditioning group after reperfusion in rats at different time points of Beclin-l and LC3-II expression decreased in different degree (P0.05) of.3 compared with sham operation group, ischemia reperfusion group and ischemic preconditioning group after reperfusion in rats at different time points Bcl-2 The expression of Caspase-3 and increased at different degrees. Compared with the ischemia-reperfusion group rats, ischemia preconditioning group rats after reperfusion, the expression of Bcl-2 in different degree (P0.05) increased, Caspase-3 expression decreased in different degree (P0.05).4 sham operation group rats had no nerve cell autophagy and apoptosis morphology after ischemia reperfusion. 2H is little autolysosome, apoptosis is not obvious; the number of 6h after ischemia reperfusion autophagy lysosome apoptosis cells showed mild changes; ischemia reperfusion 12~24h autophagy lysosome apoptosis change degree is increased, nuclear as well as massive margination of chromatin, nuclear morphology was irregular, sustained to 3D; ischemia after reperfusion, 5D is still visible. Morphology of autophagy and apoptosis in ischemic preconditioning group rats compared with ischemia reperfusion group rats, nerve cell autophagy and apoptosis occurred decreased.
Conclusion 1 cerebral ischemia reperfusion injury of nerve cells, the cell autophagy and apoptosis, manifested as nerve function and ischemic cerebral hemisphere infarction and infarction area of the nerve cells, autophagy and apoptosis related proteins Beclin-l, LC3-II, Bcl-2 and Caspase-3 expression increased significantly, the number of nerve cell autophagy lysosome and apoptosis significantly the change of.2 in cerebral ischemia preconditioning has protective effect on nerve cells, autophagy and apoptosis to decrease, to reduce neurological deficits, reduce ischemic cerebral hemisphere infarction volume and reduce the infarct area of the nerve cells, autophagy and apoptosis related proteins Beclin-l, LC3-II and Caspase-3 expression decreased, Bcl-2 expression increased significantly the number of nerve cells, reduce the cell apoptosis and autophagy lysosome, reduce the degree of change.

【學(xué)位授予單位】：河北聯(lián)合大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類(lèi)號(hào)】：R743

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本文編號(hào)：1735076