本文選題：氯化鋰 + 間充質(zhì)干細(xì)胞　； 參考：《中國病理生理雜志》2017年12期

【摘要】：目的:研究氯化鋰(Li Cl)對(duì)大鼠骨髓間充質(zhì)干細(xì)胞(MSCs)神經(jīng)分化的影響,并探討自噬通路在其中的作用。方法:體外分離培養(yǎng)大鼠骨髓間充質(zhì)干細(xì)胞,細(xì)胞分為Li Cl組和對(duì)照組,采用β-巰基乙醇誘導(dǎo)MSCs向神經(jīng)細(xì)胞分化,免疫熒光法和Western blot法檢測誘導(dǎo)后神經(jīng)元標(biāo)志蛋白神經(jīng)元特異性烯醇化酶(NSE)和微管相關(guān)蛋白2(MAP-2)以及自噬標(biāo)志蛋白微管相關(guān)蛋白1輕鏈3(LC3)的表達(dá)變化。進(jìn)一步采用自噬激活劑雷帕霉素(rapamycin)及自噬抑制劑3-甲基腺嘌呤(3-MA)干預(yù)自噬,Western blot法觀察NSE和MAP-2的表達(dá)變化。結(jié)果:誘導(dǎo)分化后,Li Cl組及對(duì)照組細(xì)胞均有NSE和MAP-2表達(dá),Li Cl組細(xì)胞NSE和MAP-2蛋白陽性表達(dá)率及表達(dá)量均大于對(duì)照組(P0.05);此外,Li Cl組細(xì)胞LC3陽性熒光點(diǎn)以及LC3-Ⅱ表達(dá)量亦多于對(duì)照組(P0.05)。加用雷帕霉素可進(jìn)一步促進(jìn)Li Cl處理的細(xì)胞NSE和MAP-2蛋白的表達(dá)(P0.05),而3-MA則抑制Li Cl處理的細(xì)胞NSE和MAP-2蛋白的表達(dá)(P0.05)。結(jié)論:氯化鋰可能通過調(diào)節(jié)自噬通路促進(jìn)大鼠骨髓骨髓間充質(zhì)干細(xì)胞向神經(jīng)細(xì)胞分化。
[Abstract]:Aim: to study the effect of LiCl on neural differentiation of rat bone marrow mesenchymal stem cells (MSCs) and to explore the role of autophagy pathway. Methods: rat bone marrow mesenchymal stem cells were isolated and cultured in vitro. The cells were divided into LiCl group and control group. 尾 -mercaptoethanol was used to induce the differentiation of MSCs into neural cells. The expression of neuron-specific enolase (NSE), microtubule-associated protein 2mAP-2 and autophagy marker microtubule-associated protein 1 light chain 3hlc 3) were detected by immunofluorescence and Western blot assay. Furthermore, autophagy activator rapamycin and autophagy inhibitor 3-methyladenine 3-MA) were used to observe the expression of NSE and MAP-2 in autophagy by Western blot assay. Results: the positive expression rate and quantity of NSE and MAP-2 protein in Li Cl group and control group were higher than those in control group (P 0.05), in addition, the positive fluorescent point of LC3 and the expression of LC3- 鈪，

本文編號(hào)：1911111