高质量浓度肿瘤坏死因子α对骨髓间充质干细胞的损伤作用

发布时间：2018-01-08 14:15

本文关键词：高质量浓度肿瘤坏死因子α对骨髓间充质干细胞的损伤作用　出处：《中国组织工程研究》2016年36期 　论文类型：期刊论文

【摘要】：背景:干细胞移植在脑缺血治疗中取得了良好效果,如何减少移植细胞的损伤成为治疗重点。目的:探讨肿瘤坏死因子α对骨髓间充质干细胞的损伤作用及可能机制。方法:原代培养SD大鼠骨髓间充质干细胞,高质量浓度肿瘤坏死因子α(200μg/L)处理6 h,MTT比色法检测细胞存活率,Hoechst33342染色观测细胞凋亡,Annexin-V/PI双染检测细胞凋亡率,丙二醛、超氧化物歧化酶试剂盒检测细胞氧化应激水平,Western blot法检测Akt、p-Akt、Fox O1及p-FoxO 1蛋白表达改变。结果与结论:(1)相比对照组,高质量浓度肿瘤坏死因子α处理6 h后,骨髓间充质干细胞存活率下降,凋亡率上升;(2)肿瘤坏死因子α作用后,G_1期和G_2期细胞比例降低,S期细胞比例增高,氧化应激水平增高,p-Akt、p-FoxO 1蛋白表达降低,差异有显著性意义(P0.05);(3)结果提示,高质量浓度肿瘤坏死因子α可诱导骨髓间充质干细胞周期阻滞,诱导凋亡,提高其氧化应激水平,其损伤机制可能与抑制Akt-FoxO 1信号通路有关。
[Abstract]:Background: stem cell transplantation has achieved good results in the treatment of cerebral ischemia. Objective: to investigate the effect of tumor necrosis factor 伪 on bone marrow mesenchymal stem cells and its possible mechanism. Methods: primary culture of SD rat bone marrow mesenchymal stem cells. Cell apoptosis was detected by MTT colorimetric assay and Hoechst33342 staining at high concentration of TNF- 伪 200 渭 g / L for 6 h. The rate of apoptosis was detected by Annexin-V/PI double staining, and the level of oxidative stress was detected by using malondialdehyde (MDA) and superoxide dismutase (SOD) kit. Western blot assay was used to detect Akt. Results compared with the control group, the expression of p-AktCon Fox O1 and p-FoxO1.Results compared with the control group, the high concentration of TNF- 伪 was treated for 6 h. The survival rate of bone marrow mesenchymal stem cells decreased and the apoptosis rate increased. (2) after the treatment of TNF- 伪, the proportion of cells in the G1 phase and the second phase of GHS decreased, while the oxidative stress level increased and the protein expression of p-Aktna-p-FoxO1 decreased. The difference was significant (P 0.05). The results suggested that high concentration of TNF- 伪 could induce cell cycle arrest, induce apoptosis and increase oxidative stress level of bone marrow mesenchymal stem cells. Its mechanism may be related to the inhibition of Akt-FoxO 1 signaling pathway.
【作者单位】：广东医科大学病理生理学教研室;
【基金】：广东省社会发展领域科技计划项目(2013B021800073) 东莞市科技局学科科研项目(2014108101049)~~
【分类号】：R743.3;R457.7
【正文快照】： 0引言Introduction相关分子机制,为将来的临床应用提供一定的实验依据。缺血性脑卒中病情的恶化往往与随后发生的脑组织局部血流量下降、脑水肿、神经元损害等相关,其中1材料和方法Materials and methods炎性反应是脑缺血再灌注损伤的重要机制之一[1-4]。1.1设计细胞学体外实

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