睾酮对心力衰竭雄性大鼠心肌组织Fas转录水平的影响

Effects of testosterone on the transcript level of Fas in postinfarction heart failure male rats' myocardium

目的:研究睾酮改善心力衰竭的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(sham组),心衰组,睾酮干预组,给予生理剂量的睾酮补充3个月,取心脏,剥离左心室,用半定量RT-PCR检测心肌组织中Fas mRNA含量的变化。结果:睾酮干预组Fas mRNA相对表达量较心衰组显著降低(0.535±0.041 vs.0.570±0.060P<0.05),但仍高于假术组(0.535±0.041 vs.0.431±0.056P<0.05)。结论:睾酮补充疗法使心肌组织Fas mRNA表达量显著下降、Fas mRNA表达量下降可能是睾酮补充疗法改善心衰的可能的分子机制之一。

Objective： To investigate the mechanism of molecular biology of testosterone improving heart failure. Methods ： The left coronary 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 physiological dose of testosterone undecanonate （TU） , group I and group Ⅱ were injected peanut oil only. The rats were sacrificed twelve weeks later and the levels of the mRNA of Fas and SERCA-2a in myocardium were measured by reversed transcript-polymerase chain reaction （RT-PCR） way. Results ： the levels of mRNA of Fas in group Ⅲ were significantly lower than group Ⅱ （0. 535 ±0. 041 vs. 0.570 ± 0. 060, P 〈 0.05 ）, hut still higher than group Ⅰ （0. 535 ± 0. 041 vs. 0. 431 ± 0. 056, P 〈 0.05 ）. Conclusion ： increase level of mRNA of Fas were involved in the molecular mechanism of improving heart failure after testosterone replecement treatment.