摘要
目的 研究血管紧张素Ⅱ (AngⅡ )和醛固酮对培养的大鼠心脏成纤维细胞Bcl 2蛋白表达的影响 ,探讨其引起心肌间质成纤维细胞数目增多的原因。方法 培养SD大鼠乳鼠心脏成纤维细胞 ,以 10 -8mol/LAngⅡ或 10 -8mol/L醛固酮作用于心脏成纤维细胞 ,2 4h后收集细胞涂片 ,进行免疫组化染色 ,观察Bcl 2蛋白的表达情况。得到阳性结果者加其拮抗剂。结果 10 -8mol/LAngⅡ对心脏成纤维细胞刺激 2 4h后 ,Bcl 2蛋白的表达呈阴性 ;10 -8mol/L醛固酮作用 2 4h后 ,Bcl 2蛋白的表达呈阳性 ,其受体拮抗剂螺旋内酯可拮抗醛固酮的作用。结论 醛固酮促进心脏成纤维细胞Bcl 2蛋白的表达 ,提示醛固酮有可能通过抑制其凋亡的途径使心脏成纤维细胞数目增多 ,这一作用是通过其核受体实现的 ;AngⅡ无类似作用 。
Objective To investigate the effect of angiotensinⅡ(AngⅡ)and aldosterone on expression of Bcl 2,an apoptosis related protein,in the cultured cardiac fibroblasts,in order to reveal the mechanism by which these two hormones induce multiplication of cardiac fibroblasts.Methods The cardiac fibroblasts of newborn SD rats were cultured and coincubated with 10 -8 mol/L AngⅡor 10 -8 mol/L aldosterone for 24 hours in the presence or absence of antagonist.The cardiac fibroblasts were collected and underwent immunohistochemical staining to find out the intensity of Bcl 2 expression.Results Bcl 2 expression in cardiac fibroblasts could not be augmented by 10 -8 mol/L AngⅡ,whereas 10 -8 mol/L aldosterone enhanced Bcl 2 expression,which could be abolished by its antagonist spironolactone.Conclusions Aldosterone stimulates the expression of apoptosis related protein Bcl 2 through the mediation of its nuclear receptor,implying that it inhibits apoptosis of cardiac fibroblasts,which may account for the hyperplasia of cardiac fibroblasts. AngⅡ has no such effect and the mechanism of its hyperplastic effect should be studied further.
出处
《中华老年心脑血管病杂志》
CAS
2000年第3期185-187,共3页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
