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神经生长因子对H9 c2心肌细胞缺氧/复氧后凋亡的保护作用及其机制

谢飞 魏珂 闵苏 郝学超 朱贤林

中国药理学通报Issue(4):506-509,510,5.
中国药理学通报Issue(4):506-509,510,5.DOI:10.3969/j.issn.1001-1978.2014.04.014

神经生长因子对H9 c2心肌细胞缺氧/复氧后凋亡的保护作用及其机制

Anti-apoptotic effect of NGF on H9 c2 cardiac myocytes in a hypoxia/reoxygenation injury model

谢飞 1魏珂 1闵苏 1郝学超 1朱贤林1

作者信息

  • 1. 重庆医科大学附属第一医院麻醉科,重庆 400016
  • 折叠

摘要

Abstract

Aim To investigate the anti-apoptotic effect of NGF on H9 c2 cardiac myocytes in a hypoxia / reox-ygenation injury model and its mechanism. Methods The H9 c2 cardiac myocytes were randomly divided into five groups:control group ( C group) , hypoxia/reoxy-genation group ( H/R group) , NGF group ( N group) , NGF+LY294002 group ( N+L group) and LY294002 group( L group) . Each group received the correspond-ing treatment. Cell survival rate was tested by cell counter kit-8 methods. Apoptotic rate was evaluated by propidium iodide ( PI ) staining and flow cytometry (FCM). The levels of Caspase-12, p-Akt/Akt were e-valuated by Western blot. Results The NGF group could significantly protect the H9 c2 cardiac myocytes under the hypoxia / reoxygenation injury with increased cell survival rate. It also decreased the apoptotic per-centage, upregulated the level of p-Akt/Akt and inhib-ited the expression of Caspase-12 . As the specific in-hibitor of PI3k receptor, LY294002 decreased the level of p-Akt. Conclusion NGF has the effect of anti-ap-optosis on H9 c2 cardiac myocytes exposed to hypoxia /reoxygenation injury via PI3k-Akt signal pathway.

关键词

H9 c2 心肌细胞/缺氧/复氧损伤/神经生长因子/PI3k-Akt通路/心肌细胞存活率/心肌细胞凋亡率/内质网应激蛋白

Key words

H9 c2 cardiac myocytes/hypoxia / reoxy-genation injury/nerve growth factor/PI3 k-Akt signal pathway/survival rate of cardiac myocytes/apoptotic percentage/endoplasmic reticulum stress protein

分类

医药卫生

引用本文复制引用

谢飞,魏珂,闵苏,郝学超,朱贤林..神经生长因子对H9 c2心肌细胞缺氧/复氧后凋亡的保护作用及其机制[J].中国药理学通报,2014,(4):506-509,510,5.

基金项目

国家自然科学基金青年基金项目( No 81000066) ( No 81000066)

卫生部国家临床重点专科[ No 财社〔2011〕170号] ()

重庆市医学重点学科建设项目[ No 渝卫科教〔2007〕2号] ()

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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