摘要
本研究在新生大鼠原代培养心肌细胞上，观察血管紧张素Ⅱ（ＡｎｇｉｏｔｅｎｓｉｎⅡ，ＡｎｇⅡ）对心肌细胞蛋白质含量和ＭＨＣ基因表达的影响。实验结果如下：（１）ＡｎｇⅡ不影响心肌细胞数目，ＡｎｇⅡ增加心肌细胞总蛋白含量和每个心肌细胞蛋白质含量，且在１０￣（－９）Ｍ～１０￣（－５）范围内呈明显剂量依赖关系，在１０￣（－６）Ｍ时达最大效应。ＡｎｇⅡ受体阻断剂Ｓａｒａｌａｓｉｎ不影响心肌细胞数目和蛋白质含量，但能阻断ＡｎｇⅡ促进蛋白质合成的作用。（２）在培养新生大鼠心肌细胞中，用１０￣（－７）ＭＡｎｇⅡ处理后，６ｈ引起α－ＭＨＣｍＲＮＡ水平迅速增加，１２ｈ达峰值，为对照组的１．７５倍（Ｐ＜０．０５）β－ＭＨＣｍＲＮＡ水平也有所增加，为对照组的１．２５倍（Ｐ＜０．０５）．两者均呈量效关系。Ｓａｒａｉａｓｉｎ可阻断ＡｎｇⅡ诱导α－ＭＨＣ和β－ＭＨＣ基因的表达，以上结果表明，ＡｎｇⅡ通过其受体介导作用，可诱导心肌细胞α－ＭＨＣ和β－ＭＨＣ基因的表达。促进蛋白质合成增加。
In this study, We determined the protein content and analy zed myosin heavy chain(MHC)gene molecular phenotype of cultured neonatal rat myocardial cell in response to Angiotensin Ⅱ(Ang Ⅱ).The results indicatedthat(1))there was no significant difference in cell numbers, while Ang Ⅱ can increase the protein content of cardiac myocytes in a dose-dependent manner. Peak response is at Ang Ⅱ concentration of 10￣(-6)M. The effect of Ang Ⅱ was blocked by specific Ang Ⅱ-receptor antagnist,Saralasin.(2)Treatment of cardiac myocytes with Ang Ⅱ(10￣-7M)for 12 hrs increased α-MHCmRNA content by 75%over the control value, and increased slightly β-MHCmRNA by 25%,Ang Ⅱ induced MHC gene expression in a dose-dependent manner in cardiac myocytes, The increases in the expression of α-MHC andβ-MHC genes induced by Ang Ⅱ were complately blocked by Saralasin.This study showed that Ang Ⅱ may increase the protein synthedes and induced MHC genes expression in cultured neonatal rat cardiac myocytes by Ang Ⅱ receptor. Ang Ⅱ may be an important humoral factor in promoting and maintaining cardiac hypertrophy,independent of secondary hemodynamic effect.
出处
《南通医学院学报》
1996年第4期468-471,共4页
ACTA Academiae Medicinae Nantong
基金
国家自然科学基金
关键词
血管紧张素Ⅱ
肌球蛋白
重链基因
心肌
细胞培养
angiotensin Ⅱ
protein content
myosin heavy chain gene
cardiac myocyte culture
