| 欧奇林，曾泗宇，骆竞妃，彭虹艳，洪陈亮，曾高峰，秦旭平.CGRP通过抑制p38MAPK/ NOX4通路保护.[J].中南医学科学杂志.,2015,43(4):374-378. |
| CGRP通过抑制p38MAPK/ NOX4通路保护 |
| Inhibition of p38MAPK / NOX4 Signal Pathway Mediates the Protection of CGRP on the HUVECs Injured by Oxidative Stress |
| 投稿时间：2015-05-08 |
| DOI： |
| 中文关键词: 降钙素基因相关肽 氧化应激 内皮细胞 NADPH氧化酶4 |
| 英文关键词:CGRP oxidative stress endothelial cell NADPH Oxidase4 |
| 基金项目:深圳市科技计划项目（201302096）；深圳市新发传染病重点专科基金. |
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| 中文摘要: |
| 目的 观察降钙素基因相关肽（CGRP）对氧化应激损伤血管内皮细胞的保护作用及其对p38 MAPK/NOX4信号通路的抑制作用。 方法 体外培养人脐静脉内皮细胞株（HUVECs），外源性给予过氧化氢（H2O2）或血管紧张素Ⅱ（Ang Ⅱ）作为氧化刺激因素，CGRP作为保护剂处理细胞。噻唑蓝比色法（MTT）观察HUVECs活力；流式细胞仪（FCM）观察分析HUVECs增殖指数的改变； Western Blot和Real-time PCR分别检测p38 MAPK、NADPH氧化酶4 （NOX4）蛋白和mRNA的表达。 结果 500 μmol/L H2O2或100 nmol/L AngⅡ能浓度依赖性地降低HUVECs活力和增殖指数（PI）；CGRP可以显著增加HUVECs活力和及其PI。同时，H2O2、AngⅡ均能诱导p38 MAPK磷酸化，并能上调NOX4蛋白和mRNA表达，p38 MAPK阻断剂能部分增强CGRP抑制AngⅡ或H2O2诱导的NOX4的表达。 结论 CGRP对内外源性的氧化应激损伤HUVECs的保护机制可能与抑制p38 MAPK/NOX4信号通路有关。 |
| 英文摘要: |
| Objective To study the protection of cacitonin gene-related peptide （CGRP） on human umbilical vein endothelial cells （HUVECs） injured by oxidative stress,and explore whether the mechanism involved in inhibition of p38MAPK/ NOX4 signal pathway. Methods HUVECs cell line were cultured in vitro,angiotensin Ⅱ （AngⅡ） or hydrogen peroxide （H2O2） serves as the gent of oxidative stress,CGRP serves as the protection agent.MTT was used to test the viability of cells,distribution of cell cycles and proliferation of cells were observed by flow cytometry.The protein or mRNA expressions of the p38 MAPK、NADPH oxidase 4 （NOX4） was measured by Western blot or RT-PCR,respectively. Rethods Compared with control group,AngⅡ or H2O2 decreased the cell viability and proliferation index （PI）dose-dependently，which were inhibited by 100 nmol/L CGRPMeantime,the level of phosphated p38 MAPK was induced by AngⅡ or H2O2,and increased the expression of NOX4.Pretreatment with CGRP and SB 203580 can inhibit the up-regulation of NOX4 induced by AngⅡ or H2O2. Conclusions The protection of CGRP on the HUVECs injured by oxidative stress from in vitro（H2O2） or in vivo（AngⅡ） is related to inhibition of p38MAPK/ NOX4 signal pathway. |
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