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首页|期刊导航|基础医学与临床|表没食子儿茶素没食子酸酯减轻LPS诱导新生大鼠原代神经胶质细胞损伤

表没食子儿茶素没食子酸酯减轻LPS诱导新生大鼠原代神经胶质细胞损伤

龙明 李晶 封玉玲 龚明 董志

基础医学与临床Issue(2):203-207,5.
基础医学与临床Issue(2):203-207,5.

表没食子儿茶素没食子酸酯减轻LPS诱导新生大鼠原代神经胶质细胞损伤

Epigallocatechin-3-gallate (EGCG) reduces the LPS-induced injury of newborn rat primary cultured glial cells

龙明 1李晶 1封玉玲 1龚明 1董志2

作者信息

  • 1. 重庆三峡医药高等专科学校附属医院神经内科,重庆404120
  • 2. 重庆医科大学药学院,重庆400016
  • 折叠

摘要

Abstract

Objective To determine the effects of EGCG on lipopolysaccharide ( LPS)-induced neuroinflamma-tion and investigate the role of neuroprotection mediated by EGCG .Methods Primary cultures of rat gliacyte were used as an in vitro model to examine the effects of EGCG on LPS-induced neuronal damage .The intracellu-lar Glu andγ-GABA were quantified via HPLC .Then the protein level of TNF-α,IL-1βand IL-8 was determined by ELISA and Western blot assay .Results Compared with the control group , LPS apparently induced the pro-duction of intracellular ROS ( P<0.05 ) and released the TNF-α, IL-1βand IL-8 in the primary cultures super-natant (P<0.05).Compared with the LPS group,EGCG significantly attenuated the release of TNF-α, IL-1βand IL-8 ( P<0.05 ) and the level of iNOS protein ( P<0.05 ) .LPS apparently induced the production of intra-cellular ROS( P<0.05 ) and released the TNF-α, IL-1βand IL-8 in the primary cultures supernatant ( P <0.05 ) .EGCG significantly attenuated the release of TNF-α, IL-1βand IL-8 ( P<0.05 ) and the level of iNOS protein(P<0.05), and rugulated the concentration of Glu/γ-GABA(P<0.05).Conclusions EGCG is effective&nbsp;in protecting hosts against LPS-induced neuroinflammation through anti-inflammatory effects and regulating extracel-lular Amino acid levels .

关键词

EGCG/脂多糖/炎性反应/氨基酸/神经保护

Key words

EGCG/lipopolysaccharide/neuroinflammation/amino acid/protection effect

分类

医药卫生

引用本文复制引用

龙明,李晶,封玉玲,龚明,董志..表没食子儿茶素没食子酸酯减轻LPS诱导新生大鼠原代神经胶质细胞损伤[J].基础医学与临床,2015,(2):203-207,5.

基金项目

重庆市基础与前沿研究计划(cstc2014jcyjA10049);重庆市卫生局医学科研项目(2012-1-096);重庆市高等教育教学改革研究重点项目(132128,133309);重庆市万州区科技计划 ()

基础医学与临床

OACSCDCSTPCD

1001-6325

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