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低氧诱导神经干细胞凋亡和 miR-26a 低表达

李芳 魏红艳 邓宇斌 李欣 李恒杰 胡春林 卢远征 廖晓星

中国病理生理杂志Issue(1):81-86,6.
中国病理生理杂志Issue(1):81-86,6.DOI:10.3969/j.issn.1000-4718.2015.01.016

低氧诱导神经干细胞凋亡和 miR-26a 低表达

Hypoxia promotes apoptosis of neural stem cells and down-regulates miR-26 a

李芳 1魏红艳 1邓宇斌 2李欣 1李恒杰 1胡春林 1卢远征 1廖晓星1

作者信息

  • 1. 中山大学附属第一医院 急诊科,广东广州510080
  • 2. 中山大学附属第一医院 转化医学中心,广东广州510080
  • 折叠

摘要

Abstract

AIM: To investigate the effect of cobalt chloride (CoCl2) on the apoptosis of neural stem cells (NSCs) and the expression of microRNA-26a (miR-26a) in vitro, and to explore the mechanisms of NSC apoptosis in-duced by CoCl 2 .METHODS:NSCs were exposed to CoCl 2 at different doses (200~600μmol/L) for 24 h.The cell via-bility and apoptosis were measured by CCK-8 assay and TUNEL method.The expression of miR-26a-3p, miR-26a-5p, GSK-3β, caspase-3, Bcl-2 and Bax was examined by real-time PCR.The protein levels of Bcl-2 and Bax were detected by Western blotting .RESULTS: The cell viability was inhibited and the apoptosis of NSCs was increased significantly by CoCl2 in a dose-dependent manner (P<0.05).CoCl2 at concentration of 400μmol/L for 24 h was used to induce apopto-sis and the expression of miR-26a was down-regulated compared with control (P<0.05).Exposure to CoCl2 at concentra-tion of 400μmol/L up-regulated the expression of GSK-3β, caspase-3 and Bax , down-regulated the expression of Bcl-2 and Bcl-2/Bax (P<0.05).CONCLUSION:CoCl2 at concentration of 400μmol/L induces the apoptosis of NSCs obviously . CoCl2 may induce the NSC apoptosis by mitochondrial apoptotic pathway .Declining miR-26a may be related to NSC apopto-sis.

关键词

氯化钴/细胞凋亡/神经干细胞/miR-26a

Key words

Cobalt chloride/Apoptosis/Neural stem cells/miR-26a

分类

医药卫生

引用本文复制引用

李芳,魏红艳,邓宇斌,李欣,李恒杰,胡春林,卢远征,廖晓星..低氧诱导神经干细胞凋亡和 miR-26a 低表达[J].中国病理生理杂志,2015,(1):81-86,6.

基金项目

国家自然科学基金资助项目 ()

中国病理生理杂志

OA北大核心CSCDCSTPCD

1000-4718

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