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首页|期刊导航|基础医学与临床|PKC/NADPH氧化应激途径对大鼠心脏微血管内皮细胞eNOS脱偶联的影响

PKC/NADPH氧化应激途径对大鼠心脏微血管内皮细胞eNOS脱偶联的影响

成永霞 刘贵波 颜彬 冯玉宽 郭素芬 王宏伟 杨向红

基础医学与临床2013,Vol.33Issue(1):82-87,6.
基础医学与临床2013,Vol.33Issue(1):82-87,6.

PKC/NADPH氧化应激途径对大鼠心脏微血管内皮细胞eNOS脱偶联的影响

Effects of PKC/NADPH oxidase on AGEs-induced eNOS uncoupling in rat cardiac microvascular endothelial cells

成永霞 1刘贵波 2颜彬 1冯玉宽 2郭素芬 1王宏伟 1杨向红3

作者信息

  • 1. 牡丹江医学院病理教研室,黑龙江牡丹江157011
  • 2. 牡丹江医学院解剖教研室,黑龙江牡丹江157011
  • 3. 中国医科大学附属盛京医院病理科,辽宁沈阳100011
  • 折叠

摘要

Abstract

Objective To observe the effects of PKC/NADPH oxidase on AGEs-induced eNOS uncoupling in rat cardiac microvascular endothelial cells. Methods To culture the cardiac microvascular endothelial cells in vitro. AGEs(100 mg/L) , DPI and LY33531 (2. 5,5 and 10 μmol/L)was respectively added and resumed incubation for 24 hrs. BH4 , NO, O-2 generation, eNOS, ROS and P47phox protein expression were examined. Results As LY33531 and DPI concentration was increased, production of NO was noted increased gradually (90. 7 ± 0. 3 ~ 122. 6 ± 0. 3,160. 6 ± 0. 6, P 〈 0. 05) , while production of 0-2 was decreased gradually (P 〈 0. 05) , BH4 expres-sion was increased(P 〈0. 05) , eNOS expression was gradually decreased ( 126. 1 ±3.5 ~112. 6 ±1.7,114. 4 ± 1.7,P〈0. 05). Meanwhile, P47phox protein expression and ROS decreased gradually (P〈0. 05). Conclusions AGEs may trigger the activation of PKC/NADPH oxidative stress pathway inducing intracellular eNOS uncoupling in cardiac microvascular endothelial cells.

关键词

糖基化终末产物/心脏微血管内皮细胞/一氧化氮/内皮型一氧化氮合酶/PKC/NADPH/LY33531/DPI

Key words

BSA-AGEs/ cardiac microvascular endothelial cells/ NO/ eNOS/ PKC/NADPH/LY33531/DPI

分类

医药卫生

引用本文复制引用

成永霞,刘贵波,颜彬,冯玉宽,郭素芬,王宏伟,杨向红..PKC/NADPH氧化应激途径对大鼠心脏微血管内皮细胞eNOS脱偶联的影响[J].基础医学与临床,2013,33(1):82-87,6.

基金项目

教育部科学技术研究重点项目(211050) (211050)

黑龙江省青年科学基金(QC2010040) (QC2010040)

基础医学与临床

OA北大核心CSCDCSTPCD

1001-6325

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