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作 者:汪晨净[1] 刘俊田[2] 郭芳[2] 南晓东 赵晋[1]
机构地区:[1]西北民族大学医学院机能教研室,甘肃兰州730030 [2]西安交通大学医学院药理系,陕西西安710061 [3]武警甘肃总队医院急诊科,甘肃兰州730050
出 处:《西安交通大学学报(医学版)》2012年第3期295-299,共5页Journal of Xi’an Jiaotong University(Medical Sciences)
基 金:西北民族大学中青年科研基金(No.XBMU-2010-BD-4);高等学校博士学科点专项科研基金资助项目(No.20100201110053)~~
摘 要:目的观察内皮素-1(ET-1)诱导血管平滑肌细胞(VSMCs)产生C-反应蛋白(CRP)的作用及其机制。方法培养大鼠VSMCs,以不同浓度ET-1刺激VSMCs,并用ETA拮抗剂BQ123、抗氧化剂PDTC、p38MAPK抑制剂SB203580及ETB阻断剂BQ788进行干预,免疫细胞化学法及半定量逆转录聚合酶链反应(RT-PCR)法分别测定不同浓度及不同干预因素下VSMCs中CRP蛋白及mRNA的表达。结果 ET-1能刺激VSMCs CRP蛋白及mRNA的表达增强,其效应呈浓度依赖性;BQ123、PDTC及SB203580能明显减少ET-1诱导的大鼠VSMCs CRP蛋白及mRNA的表达,而BQ788对此作用无明显影响。结论 ET-1通过ETA、活性氧(ROS)、p38MAPK诱导大鼠VSMCs产生CRP。Objective To observe the effect of endothelin-1(ET-1) on C-reactive protein(CRP) generation in rat vascular smooth muscle cells(VSMCs) and the primary mechanisms.Methods Rat VSMCs were cultured.CRP protein expression stimulated with ET-1 was examined with the immunocytochemical method,and CRP mRNA expression was identified with the semi-quantitative reverse transcription polymerase chain reaction(RT-PCR).Results ET-1 stimulated CRP generation in VSMCs at both protein and mRNA levels in a dose-dependent manner.ETA receptor antagonist BQ123,but not ETB receptor antagonist BQ788,inhibited ET-1-stimulated mRNA and protein expressions of CRP in VSMCs.In addition,antioxidant pyrrolidine dithiocarbamate and p38MAPK inhibitor SB203580 reduced ET-1-induced mRNA and protein expressions of CRP.Conclusion ET-1 induces CPR production in rat VSMCs via ETA receptor and subsequent ROS and MAPK signal pathway.
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