N-乙酰半胱氨酸通过激活PI3K-Akt信号途径抑制过氧化氢诱导骨髓间充质干细胞凋亡

中国生物工程杂志

2013, Vol. 33

Issue (11): 1-7

研究报告

N-乙酰半胱氨酸通过激活PI3K-Akt信号途径抑制过氧化氢诱导骨髓间充质干细胞凋亡

谢荣辉^1,2, 殷嫦嫦³, 殷明¹, 陈伟才¹, 邬亚华³, 何丁文^1,2, 林思文^1,2, 耿书国^1,2

1 南昌大学第二附属医院南昌 330006;
2 南昌大学研究生院医学部南昌 330006;
3 九江学院九江 332000

N-acetyl-L-cysteine Protect BMCSs Against Apoptosis Induced by H₂O₂ Via Regulaing the Activity of PI3K-Akt Signaling Pathways

XIE Rong-hui^1,2, YIN Chang-chang³, YIN Ming¹, CHEN Wei-cai¹, WU Ya-hua³, HE Ding-wen^1,2, LIN Si-wen^1,2, GENG Shu-guo^1,2

1 The Second Affiliated Hospital of Nanchang University, Nanchang 330006, China;
2 Nanchang University Graduate School of Medicine, Nanchang 330006, China;
3 Jiujiang University, Jiujiang 332000, China

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摘要： 目的：研究N-乙酰半胱氨酸（NAC）对H₂O₂诱导骨髓间充质干细胞（BMSCs）凋亡的影响，并探讨N-乙酰半胱氨酸对骨髓间充质干细胞的PI3K-Akt信号通路的影响。方法：采用全骨髓贴壁培养法培养SD大鼠BMSCs，随机分成5组：正常对照组、H₂O₂处理组、NAC组、NAC+H₂O₂组和LY294002干预组。倒置相差显微镜观察各组细胞形态变化；MTT法检测不同浓度H₂O₂、NAC刺激组细胞存活率；流式细胞术检测各组的细胞凋亡率；Western blot检测各组rBMSCs中Akt，p-Akt的表达。结果：H₂O₂可诱导BMSCs发生凋亡，其存活率与H₂O₂浓度呈依赖性改变，其形态呈典型的凋亡样改变；与H₂O₂组相比，正常对照组、NAC+H₂O₂组的凋亡率均降低；与LY294002干预组相比，NAC+H₂O₂组的凋亡率降低，H₂O₂组与之没有统计学差异；与正常组相比，NAC能刺激磷酸化Akt水平升高，并与作用时间长短有关；与H₂O₂组相比，NAC+H₂O₂组的p-Akt表达量升高，而LY294002干预组与H₂O₂组的p-Akt表达量未见明显差异。结论：N-乙酰半胱氨酸可通过激活PI3K-Akt信号通路对过氧化氢诱导的骨髓间充质干细胞凋亡起到保护作用。

关键词： N-乙酰半胱氨酸; 骨髓间充质干细胞; 凋亡; PI3K-Akt信号通路; 过氧化氢

Abstract: Objective: To study whether the N-acetyl cysteine (NAC) has direct cytoprotective effects on bone marrow mesenchymal stem cells (BMSCs) against apoptosis induced by H₂O₂ and and if the PI3K-Akt has partticipated in the mechanism of anti-apoptosis.Methods: BMSCs were extracted from SD rats and cultured by whole bone marrow adherence method. cultured cells were randomly divided into normal control group, H₂O₂ treatment group, the NAC group, NAC + H₂O₂ group and LY294002 intervention group. Then the cellular morphology was observed under inverted phase contrast microscope; Cell survival rate of BMSCs was determined by MTT assay in the different concentration of H₂O₂and NAC; The apoptosis rate of BMSCs was detected by flow cytometry;the expressions of p-Akt and Akt were analyzed by Western blot.Results The apoptosis of BMSCs could be induced by H₂O₂,its cell survival rate occurred coincident with H₂O₂concentrations,and its morphology appears typical apoptotic characteristic.Compared with H₂O₂ group,the rate of apoptosis between normal control group and NAC+H₂O₂ group were lower;but in LY294002 intervention group,its rate of apoptosis was higher and has no significant difference as compared with that of H₂O₂ group;Compared with normal group, NAC could increase the expression levels of p-Akt and be related to time of exposure; Compared: with H₂O₂ group,the expression of p-Akt increased,there was no significant difference between H₂O₂ group and LY294002 intervention group.Conclusion: N-acetyl-L-cysteine can protect the BMCSs against apoptosis induced by H₂O₂ via the activation of PI3K-Akt signaling pathways.

Key words: N-acetyl-L-cysteine Hydrogen peroxide Bone marrow-derived mesenchymal stemcells Apoptosis PI3K-Akt signalling pathway

收稿日期: 2013-08-28 出版日期: 2013-11-25

ZTFLH:

R273

基金资助: 江西省教育厅科技课题资助项目（GJJ13740）

通讯作者: 殷嫦嫦 E-mail: yinchangchang112@163.com

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引用本文:

谢荣辉, 殷嫦嫦, 殷明, 陈伟才, 邬亚华, 何丁文, 林思文, 耿书国. N-乙酰半胱氨酸通过激活PI3K-Akt信号途径抑制过氧化氢诱导骨髓间充质干细胞凋亡[J]. 中国生物工程杂志, 2013, 33(11): 1-7.

XIE Rong-hui, YIN Chang-chang, YIN Ming, CHEN Wei-cai, WU Ya-hua, HE Ding-wen, LIN Si-wen, GENG Shu-guo. N-acetyl-L-cysteine Protect BMCSs Against Apoptosis Induced by H₂O₂ Via Regulaing the Activity of PI3K-Akt Signaling Pathways. China Biotechnology, 2013, 33(11): 1-7.

链接本文:

https://manu60.magtech.com.cn/biotech/CN/ 或 https://manu60.magtech.com.cn/biotech/CN/Y2013/V33/I11/1

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