摘要
目的:探讨睾酮改善心力衰竭可能的分子生物学机制。方法:建立心衰模型,将大鼠随机分为假手术组、心衰组和睾酮干预组(给予生理剂量的睾酮补充),3个月后处死动物,取心脏,2剥离左心室,用半定量RT-PCR检测心肌组织中SERCA-2 a mRNA含量的变化。结果:睾酮干预组SERCA-2 a mRNA相对表达量较心衰组升高(0.516±0.075 vs 0.428±0.062,P<0.05),但依然低于假术手组(0.516±0.075 vs 0.572±0.063,P<0.05)。结论:睾酮可使心肌组织SERCA-2 amRNA含量上升,睾酮补充疗法可能是改善心衰的分子机制之一。
Objective： To investigate the mechanism of molecular biology of testosterone improving heart failure. Methods ： The left coronary artery of male Sprague-Dawley rat was ligated to create a myocardial infarct model, six weeks later, the qualified animals were randomized into two groups, heart failure group（group Ⅱ n = 22）, hear failure ＋ testosterone group （ group Ⅲ n = 22）, Sham operated rats were used as control （group Ⅰ n = 15） , group Ⅲ was injected by physiological dose of testosterone undecanonate（TU） , group Ⅰ and group Ⅱwere injected by peanut oil only. The rats were sacrificed twelve weeks later and the levels of the mRNA of SERCA-2a in myocardium were measured by reversed transcript-polymerase chain reaction （RT-PCR） way. Results： The levels of mRNA of SERCA-2a in group Ⅲwere higher than group Ⅱ（0. 516 ± 0. 075 vs 0. 428 ± 0.062, P 〈0.05）, but lower than those of group Ⅰ （0. 516 ± 0. 075 vs 0. 572 ± 0.063, P 〈 0.05）. Conclusion ： Declining of mRNA of SERCA-2a were involved in the molecular mechanism of improving heart failure after testosterone replecement treatment.
出处
《河南医学研究》
CAS
2008年第2期113-115,共3页
Henan Medical Research
