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PICK1在肝纤维化中的表达变化及功能研究

陈培杰 李俊 黄成 孟晓明 蔡双朋

安徽医科大学学报Issue(11):1606-1609,1610,5.
安徽医科大学学报Issue(11):1606-1609,1610,5.

PICK1在肝纤维化中的表达变化及功能研究

The expression and effect of PICK1 in liver fibrosis

陈培杰 1李俊 2黄成 3孟晓明 1蔡双朋2

作者信息

  • 1. 安徽医科大学 药学院,合肥 230032
  • 2. 安徽医科大学 肝病研究所,合肥 230032
  • 3. 安徽医科大学 安徽省创新药物产业共性研究院,合肥 230032
  • 折叠

摘要

Abstract

Objective To explore the expression of protein interacting with Ca-kinase-1(PICK1)in fibrotic liver of mice and activated hepatic stellate cell,and investigate the effect of PICK1 on the activation of hepatic stellate cell strain (LX-2).Methods Liver fibrosis model in mice was induced by CCl4 and then the PICK1 level was detec-ted in fibrotic liver tissue.LX-2 cells were activated by transforming growth factor β1 (TGF-β1),and the protein level of PICK1 was detected by Western blot.After transfected with the plasmid expressing PICK1,LX-2 was stim-ulated with TGF-β1,the levels of α-smooth muscle actin(α-SMA),collagen type I (Col1a1 ),Smad2,3 and phosphorylation level of them were determined by Western blot.Results PICK1 was highly expressed in normal liver tissues and progressively down-regulated as liver fibrosis progressed.The expression of PICK1 was down-regu-lated in activated LX-2 induced by TGF-β1.The hepatic stellate cell transfected with PICK1-plasmid showed re-markablely decreased TGF-β1-induced α-SMA and Col1a1 expression and obviously declined phosphorylation levels of Smad2 and Smad3.Conclusion The expression of PICK1 decreases in fibrotic livers and activated hepatic stel-late cell.Over-expression of PICK1 can suppress the activation of hepatic stellate cell induced by TGF-β1,and probably because of the inhibitory effect on TGF-β/Smad pathway,which provides new ideas and targets for the prevention and treatment of liver fibrosis.

关键词

PICK1/肝纤维化/肝星状细胞

Key words

PICK1/Liver Fibrosis/hepatic stellate cell

分类

医药卫生

引用本文复制引用

陈培杰,李俊,黄成,孟晓明,蔡双朋..PICK1在肝纤维化中的表达变化及功能研究[J].安徽医科大学学报,2015,(11):1606-1609,1610,5.

基金项目

国家自然科学基金(编号81273526、81473268);安徽省重点科技攻关项目(编号1301042212);安徽省自然科学基金(编号1308085MH145);高等学校博士学科点专项科研基金 ()

安徽医科大学学报

OA北大核心CSTPCD

1000-1492

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