论文部分内容阅读
目的观测17β-雌二醇(17β-estradiol,E2)对肾上腺素(PE)诱导的乳鼠心肌细胞肥大的影响并探讨其机制。方法以培养的乳鼠心肌细胞为模型并分组给药,用计算机图像分析软件测量心肌细胞表面积,[3H]标记亮氨酸掺入法测定心肌细胞蛋白质合成速率,免疫细胞化学方法检测心肌细胞原癌基因c-fos蛋白表达,半定量RT-PCR检测心肌细胞肥大特征性胚胎型基因β-肌球蛋白重链(β-MHC)、α-骨骼肌肌动蛋白(α-skA)和心房肽(ANP)的mRNA表达。结果17β-雌二醇明显抑制肾上腺素诱导的心肌细胞表面积和蛋白质合成速率的增加;17β-雌二醇减弱肥大心肌细胞c-fos蛋白表达;17β-雌二醇降低β-MHC、α-skA的mRNA表达,但增加ANP mRNA表达。结论17β-雌二醇可抑制心肌细胞肥大,其作用机制可能与抑制原癌基因c-fos的蛋白表达,逆转收缩蛋白基因(β-MHC和α-skA)向胚胎型转化及促进ANP mRNA表达有关。
Objective To observe the effect of 17β-estradiol (E2) on cardiomyocyte hypertrophy induced by epinephrine (PE) in rats and its mechanism. Methods The cultured neonatal rat cardiomyocytes were used as model and administered in groups. The surface area of cardiomyocytes was measured by computer image analysis software. [3H] labeled leucine incorporation method was used to determine the rate of cardiomyocyte protein synthesis. The cytotoxicity of cardiomyocytes The expression of oncogene c-fos protein was detected by semi-quantitative RT-PCR. The expression of β-MHC, α-SMA and atrial natriuretic peptide (ANP) mRNA expression. Results 17β-estradiol significantly inhibited the epinephrine-induced increase of myocardial cell surface area and protein synthesis rate; 17β-estradiol decreased the expression of c-fos protein in hypertrophic cardiomyocytes; 17β-estradiol decreased β-MHC and α-skA MRNA expression, but increased ANP mRNA expression. Conclusion 17β-estradiol can inhibit cardiomyocyte hypertrophy and its mechanism may be related to inhibition of proto-oncogene c-fos protein expression, reversal of contractile protein gene (β-MHC and α-skA) into the embryo-type transformation and promote ANP mRNA expression related.