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首页|期刊导航|重庆医学|PI3K/Akt 信号通路在严重烧伤大鼠血清诱导 BMSCs 迁移中的作用

PI3K/Akt 信号通路在严重烧伤大鼠血清诱导 BMSCs 迁移中的作用

李茂华 滕苗 果磊

重庆医学Issue(27):3752-3755,4.
重庆医学Issue(27):3752-3755,4.DOI:10.3969/j.issn.1671-8348.2015.27.003

PI3K/Akt 信号通路在严重烧伤大鼠血清诱导 BMSCs 迁移中的作用

Role of PI3K/Akt signal pathway in BMSCs migration induced by serum of rats with severely burn

李茂华 1滕苗 1果磊1

作者信息

  • 1. 重庆医科大学附属第一医院烧伤整形外科 400016
  • 折叠

摘要

Abstract

Objective To study the effects of severely burned rats serum on migration of BMSCs and mechanism.Methods Severely burned rats model was established,and the preparation of severely burned rats serum.Experimental groups:normal train-ing group(containing 10% fetal bovine serum,group C),burn serum group(containing 10% burns in the rat serum,group B),burn serum+blockers(10% burns in the rat serum+final concentration of 10 μmol/L PI3K signaling pathway inhibitor LY294002 train-ing,group B+LY).Activity of cells was examined with MTT;migration of cells was examined with Transwell chambers testing;protein expression of p-AKT/AKT was determined with Western blot;microtubule structure of cells was examined with immuno-fluorescence.Results Compared with group C,group B burn serum treatment after 24 h,BMSCs activity(P <0.01),p-AKT levels (P <0.05),increased migration quantity(P <0.001);cell microtubule structures appear rupture,after adding inhibitor,compared with group B,group B+LY BMSCs activity(P <0.01),to reduce the number of migration(P <0.001),p-lower AKT(P <0.05), cell microtubule structure similar to the normal group.Conclusion Severely burned rats serum can promote BMSCs migration,may burn serum cytokine activation of PI3K/AKT signal pathway,resulting in cell microtubule structure change,promote the migration of BMSCs.

关键词

烧伤/间质干细胞/微管/迁移/PI3K/Akt/信号通路

Key words

burns/mesenchymal stem cells/microtubules/migration/PI3K/Akt/signaling pathway

分类

医药卫生

引用本文复制引用

李茂华,滕苗,果磊..PI3K/Akt 信号通路在严重烧伤大鼠血清诱导 BMSCs 迁移中的作用[J].重庆医学,2015,(27):3752-3755,4.

基金项目

重庆市基础与前沿研究计划项目(cstc2013jcyjA10069) (cstc2013jcyjA10069)

重庆医学

OA北大核心CSTPCD

1671-8348

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