本文選題：低氧 + PIK/AKT信號(hào)通路　； 參考：《中國(guó)病理生理雜志》2016年05期

【摘要】：目的:探討低氧預(yù)處理對(duì)老年人骨髓間充質(zhì)干細(xì)胞(h BM-MSCs)的保護(hù)作用,為提高老年自體干細(xì)胞移植治療效果提供實(shí)驗(yàn)支持。方法:老年h BM-MSCs于低氧培養(yǎng)箱中培養(yǎng)24 h進(jìn)行低氧預(yù)處理,實(shí)驗(yàn)分為年輕h BM-MSCs組(young組),老年h BM-MSCs組(old組)及低氧預(yù)處理老年h BM-MSCs組(old+hypoxia組)。300μmol/L H_2O_2作用30 min建立細(xì)胞氧化應(yīng)激模型,50μmol/L LY294002作用2 h阻斷PI3K/AKT信號(hào)通路,Brd U摻入實(shí)驗(yàn)檢測(cè)細(xì)胞增殖能力;CCK-8法檢測(cè)細(xì)胞活力,Western blot檢測(cè)凋亡相關(guān)蛋白Bax、Bcl-2表達(dá)水平和AKT磷酸化水平。結(jié)果:Brd U摻入實(shí)驗(yàn)顯示低氧預(yù)處理的老年h BM-MSCs細(xì)胞陽(yáng)性率為39.85%±3.45%,與old組相比增殖能力顯著提高(P0.05)。300μmol/L H_2O_2作用30 min誘導(dǎo)細(xì)胞氧化應(yīng)激后,old+hypoxia組與old組比較,細(xì)胞活力顯著提高(P0.05),凋亡相關(guān)蛋白Bax表達(dá)量顯著降低(P0.05),抑制凋亡的Bcl-2蛋白表達(dá)量顯著增高(P0.05),且AKT磷酸化水平顯著增高,差異有統(tǒng)計(jì)學(xué)顯著性(P0.05);應(yīng)用LY294002抑制PI3K/AKT信號(hào)通路后,細(xì)胞活力下降(P0.05)。結(jié)論:低氧預(yù)處理可以通過激活A(yù)KT信號(hào)通路提高老年人骨髓間充質(zhì)干細(xì)胞活力及增殖能力。
[Abstract]:Objective: to investigate the protective effect of hypoxic preconditioning on bone marrow mesenchymal stem cells (BM-MSCs) in the elderly and to provide experimental support for the treatment of autologous stem cell transplantation. Methods: the aged BM-MSCs was cultured in hypoxia incubator for 24 hours. The experiment was divided into three groups: young group in young BM-MSCs group, BM-MSCs group in old age group (n = 30 min) and hypoxia preconditioning group in old BM-MSCs group (n = 30 min). The model of cell oxidative stress was induced by 50 渭 mol/L LY294002 for 2 h to block the signal pathway of PI3K/AKT. The cell viability was detected by CCK-8 method. The expression of apoptosis related protein Baxfen Bcl-2 and the level of AKT phosphorylation were detected by Western blot. Results the positive rate of BM-MSCs cells was 39.85% 鹵3.45% after hypoxia preconditioning. Compared with old group, the proliferation ability of old group was significantly higher than that of old group. Compared with old group, the proliferation ability of hypoxia group was significantly higher than that of old group after 30 min induction of oxidative stress. The cell viability was increased significantly (P 0.05), the expression of apoptosis-related protein (Bax) was significantly decreased, the expression of Bcl-2 protein was significantly increased (P 0.05), and the level of AKT phosphorylation was significantly increased (P 0.05). The cell viability was decreased by P0.05. Conclusion: hypoxia preconditioning can enhance the activity and proliferation of bone marrow mesenchymal stem cells by activating AKT signaling pathway.
【作者單位】： 山西醫(yī)科大學(xué)人體解剖學(xué)教研室;山西醫(yī)科大學(xué)形態(tài)學(xué)實(shí)驗(yàn)室;山西醫(yī)科大學(xué)第二醫(yī)院;
【基金】：山西醫(yī)科大學(xué)青年基金資助項(xiàng)目(No.02201002);山西醫(yī)科大學(xué)基礎(chǔ)醫(yī)學(xué)院331基金資助項(xiàng)目(No.201217)
【分類號(hào)】：R457.7

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