雄激素对糖皮质激素所致大鼠骨骼肌萎缩的治疗作用

Therapeutic effect of androgen on skeletal muscle atrophy induced by glucocorticoid in rat

目的研究睾酮对地塞米松所致大鼠骨骼肌萎缩的治疗作用以及与胰岛素样生长因子1(IGF-1)表达的关系。方法40只雌性SD大鼠随机均分为对照组、地塞米松组、睾酮组、睾酮+地塞米松组,每日检测大鼠体重,末次给药24h后处死动物,冻存血浆标本,分离腓肠肌、称重并冻存。采用定量PCR检测腓肠肌中IGF-1 mRNA的表达,ELISA法检测血浆中IGF-1蛋白水平。结果睾酮可减轻地塞米松所致的大鼠体重与骨骼肌重量降低(P<0.01),拮抗地塞米松引起的骨骼肌中IGF-1 mRNA水平下降(P<0.01),但对血浆中IGF-1蛋白水平无明显影响。结论睾酮可减轻地塞米松所致的大鼠骨骼肌萎缩,对骨骼肌中IGF-1表达的调控可能是雄激素治疗作用的机制之一。

Objective To study the therapeatic effect of testosterone on skeletal muscle atrophy induced by dexamethasone in rat, and to explore the relationship between androgen and insulin like growth factor 1 （IGF-1） expression in skeletal muscle and serum. Methods Forty female Sprague-Dawley rats were randomly divided into four groups： control group （CON） in which the rats were injected with saline and sesame oil for 10 days; dexamethasone group （DEX） in which the rats were injected with dexamethasone and sesame oil for 10 days; testosterone group （TES） in which the rats were injected with saline and testosterone for 13 days; and the testosterone＋ dexamethasone group （TES＋DEX） in which the rats were injected with dexamethasone and testosterone. The animals were weighed daily. 24 hours following the final injection, animals were weighed and sacrificed. Blood samples were withdrawn from the abdominal aorta and centrifuged at 3 000r/min for 10min The supernatant was collected and stored at --20℃. Gastrocnemius muscle was removed, weighed and stored at --80℃. IGF 1 mRNA expression in skeletal muscle was determined by real-time PCR. IGF-1 protein expression in serum was determined by enzyme-linked immunosorbent assay （ELISA）. Results Testosterone attenuated the body weight loss and gastrocnemius muscle weight loss in rats as a result of dexamethasone adminishation （P〈0. 01）. Testosterone prevented the decline of IGF-1 mRNA expression induced by dexamethasone in gastrocnemius muscle （P〈0. 01）, but not in serum. Conclusion The results suggest that testosterone can attenuate muscle atrophy induced by dexamethasone in rat, and regulation of the expression of IGF 1 in skeletal muscle by testosterone may be involved in its mechanism.