Intermedin_(1-53)对大鼠心肌成纤维细胞增殖的影响  

Effect of intermedin_(1-53) on aldosterone-induced cardiac fibroblast proliferation

作　　者：薛立华[1] 梁颖[1] 宋君秋[2] 齐永芬[2] 贾月霞[1] 

机构地区：[1]宁夏医科大学基础医学院病理生理学系,宁夏银川750004 [2]北京大学医学部生理与病理生理学系,北京100083

出　　处：《中国病理生理杂志》2011年第11期2056-2060,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30860372)

摘　　要：目的:研究intermedin1-53(IMD1-53)对醛固酮(ALD)促SD乳鼠心肌成纤维细胞(CFBs)增殖的影响及细胞外信号调节激酶(ERK)信号转导途径的作用。方法:分离培养SD乳鼠CFBs,将细胞分成对照组、不同浓度ALD组、ALD+不同浓度IMD1-53组,用MTT比色法测定细胞活性。通过Western blotting方法观察IMD1-53对ALD诱导的p-ERK蛋白表达的影响。结果:(1)IMD1-53对基础状态下的CFBs增殖无明显抑制作用,但能呈浓度(10-9～10-7mol/L)依赖性地抑制ALD刺激CFBs的增殖。(2)IMD1-53具有浓度(10-9～10-7mol/L)依赖性地抑制ALD诱导的p-ERK蛋白表达的作用。结论:IMD1-53通过ERK信号途径抑制ALD促CFBs增殖的效应。AIM： To investigate the roles of intermedin1-53（IMD1-53） and exteracellular signal-regulated kinase（ERK） signal pathway in the proliferation of rat cardiac fibroblasts（CFBs）.METHODS： Isolated and cultured CFBs from new born SD rats were randomly divided into control group,aldosterone（ALD） groups（at different concentrations） and ALD＋IMD groups（IMD at different concentrations）.The viability of CFBs was determined by MTT assay.Western blotting was used to observe the effect of IMD on ALD-induced ERK phosphorylation.RESULTS： IMD1-53 had no significant effect on the proliferation of CFBs in basal state,but inhibited the CFBs growth stimulated by ALD in a concentration（10-9~10-7 mol/L）-dependent manner.IMD1-53 also inhibited ERK phosphorylation stimulated by ALD in a concentration（10-9~10-7 mol/L）-dependent manner.CONCLUSION： IMD1-53 inhibits the proliferation of CFBs by ERK signal pathway.

关 键 词：Intermedin1-53 心肌成纤维细胞 醛固酮 ERK通路 

分 类 号：R363[医药卫生—病理学]