摘要
目的 探讨醛固酮诱导心肌成纤维细胞 (CFs)增殖及对一氧化氮合酶 —氧化氮 (NOS NO)系统活性的影响。方法 采用胰酶消化法分离培养新生SD大鼠CFs,采用MTT比色法、硝酸还原酶法、分光光度法和半定量RT PCR技术 ,观察不同浓度醛固酮对CFs的增殖、NO含量、NOS活性和iNOSmRNA表达的影响。结果 1× 10 -11～ 1× 10 -7mol/L的醛固酮能明显促进CFs的增殖 ,且呈剂量依赖方式 ;不同浓度醛固酮干预下CFs的NO含量、NOS活性及iNOSmRNA表达逐渐下降 (P均 <0 0 5 ) ,呈剂量依赖性 ;醛固酮干预下NO含量随NOS活性降低而降低 ,二者呈显著正相关 (r=0 95 8,P <0 0 1) ;螺内酯能阻断醛固酮诱导的CFs的NO含量、NOS活性和iNOSmRNA表达下降。结论 醛固酮能剂量依赖性地降低CFs的NOS NO系统活性 ,螺内酯能逆转此作用 ,可能是其致心肌纤维化的机制之一。
Objective To investigate the changes in nitric oxide synthase (NOS) activity in cardiac fibroblasts (CFs) of neonatal rat induced by aldosterone. Method CFs were isolated by trypsin digestion method. Proliferation of CF was assessed by MTT colorimetric assay. Nitric acid reductase method and spectrophotometry were used to determine the NO contents and NOS activity, respectively, at different time after CFs being treated with aldosterone. Result Aldosterone (1×10 -11 -1×10 -7 mol/L) could increase CFs proliferation in a dose-dependent manner. NO contents, NOS activity and iNOS mRNA were decreased in a dose-dependent manner after being treated with aldosterone in different concentrations (P<0.05). NO contents declined along with decrease in NOS activity in CFs after being treated with aldosterone in different concentrations, and there was significant positive correlation between them (r=0.958, P<0.01). The effects of aldosterone on CFs were inhibited by spironolactone. Conclusion The results suggested that aldosterone suppresses NOS-NO system activity in neonatal rat CFs via mineralocorticoid receptor. The suppression of iNOS-NO system activity could be related to myocardial fibrosis induced by aldosterone.
出处
《解放军医学杂志》
CAS
CSCD
北大核心
2005年第2期142-144,共3页
Medical Journal of Chinese People's Liberation Army
