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首页|期刊导航|南方医科大学学报|普伐他汀对P38MAPK信号通路介导的胰岛微血管内皮细胞炎症损伤的保护作用

普伐他汀对P38MAPK信号通路介导的胰岛微血管内皮细胞炎症损伤的保护作用

胡南 孙嘉 康远程 陈建生 罗丽珊 张菊嫦 陈松源 蔡德鸿

南方医科大学学报2013,Vol.33Issue(8):1232-1235,1239,5.
南方医科大学学报2013,Vol.33Issue(8):1232-1235,1239,5.DOI:10.3969/j.issn.1673-4254.2013.08.30

普伐他汀对P38MAPK信号通路介导的胰岛微血管内皮细胞炎症损伤的保护作用

Protective effects of pravastatin against P38MAPK signaling pathway-mediated inflammatory toxicity in islet microendothelial cells

胡南 1孙嘉 2康远程 1陈建生 1罗丽珊 1张菊嫦 1陈松源 2蔡德鸿2

作者信息

  • 1. 南方医科大学第二临床医学院,广东广州510282
  • 2. 南方医科大学珠江医院内分泌科,广东广州510282
  • 折叠

摘要

Abstract

Objective To study the signaling pathways associated with lipopolysaccharide (LPS)-induced inflammation in islet microendothelial cells (IMECs) and the mechanism of pravastatin intervention.Methods IMECs exposed to LPS,SB203580,pravastatin,or SB203580 + pravastatin were examined for cell apoptosis with Hoechst staining and flow cytometry and for expression levels of total-p38,photophosphorylation-p38 (p-p38) and iNOS with Western blotting.Results The apoptosis rate and expression levels of total-p38,p-p38,iNOS in IMECs all increased after LPS exposure.Pravastatin,SB203580,and their combination significantly attenuated LPS-induced enhancement of cell apoptosis and total-p38,p-p38,and iNOS expressions in IMECs.Conclusion LPS-induced inflammatory toxicity in IMECs is associated with the activation of P38MAPK and iNOS/NO signaling pathways.Pravastatin can inhibit these pathways and suppress the apoptosis and necrosis of IMECs to relieve the cell inflammatory injuries.

关键词

胰岛微血管内皮细胞/普伐他汀/炎症/P38MAPK

Key words

islet microendothelial ceils/pravastatin/inflammation/P38MAPK

引用本文复制引用

胡南,孙嘉,康远程,陈建生,罗丽珊,张菊嫦,陈松源,蔡德鸿..普伐他汀对P38MAPK信号通路介导的胰岛微血管内皮细胞炎症损伤的保护作用[J].南方医科大学学报,2013,33(8):1232-1235,1239,5.

基金项目

广东省"大学生创新实验计划"项目(1212111004) (1212111004)

国家级大学生创新创业训练计划项目(201212121081) (201212121081)

广东省医学科研基金(2011B031800086) (2011B031800086)

广东省自然科学基金博士科研启动基金(S2012040006903) (S2012040006903)

广东省科技计划项目(C1030491) (C1030491)

南方医科大学学报

OA北大核心CSCDCSTPCD

1673-4254

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