【摘要】 目的:探讨创伤失血性休克复苏后大鼠生长激素-胰岛素样生长因子-1(GH-IGF-1)轴的变化以及对大鼠骨骼肌蛋白质代谢的影响。方法:将大鼠随机分为假手术组(对照组,n=9)和创伤失血性休克复苏组(模型组,n=11)。观察大鼠血清GH、游离IGF-1、胰岛素样生长因子结合蛋白3(IGFBP-3)、IGFBP-1水平和腓肠肌蛋白激酶B(PKB/Akt)-雷帕霉素靶蛋白(mTOR)信号通路的表达情况。同时检测肌肉3-甲基组氨酸(3-MH)含量。结果:模型组大鼠血清游离IGF-1水平急剧下降(P<0.01),伴随着IGFBP-3水平显著降低(P<0.01)和IGFBP-1水平明显升高(P<0.01)。IGF-1下游信号通路中Akt、mTOR和核糖体S6蛋白激酶1(S6K1)的磷酸化过程较对照组显著被抑制(P<0.01,P<0.05,P<0.05)。创伤失血性休克复苏后大鼠肌肉3-MH释放量也明显增加(P<0.01)。结论:重度创伤后出现的GH-IGF-1轴功能紊乱,引起骨骼肌蛋白质代谢异常是导致肌肉消耗的重要原因之一。更多还原

【Abstract】 Objective: To investigate the change of the growth hormone-insulin-like growth factor-1( GH-IGF-1) axis function in a rat model of trauma-hemorrhagic shock resuscitation( T / HS),and discuss the impact to the muscle protein metabolism. Methods: Male Sprague-Dawley rats were randomly assigned to 2 groups: shame( n = 9) and T / HS( n = 11). Samples were collected to determine the serum levels of free IGF-1,IGFBP-3,and IGFBP-1. Phosphorylations of mammalian target of rapamycin( mTOR) related anabolic signaling pathway and muscle 3-methyl histidine( 3-MH) levels were also detected. Results: Rats serum levels of free IGF-1 and IGFBP-3 dramatically decreased after T / HS( P < 0. 01,P < 0. 01),accompanying with the significant increase in IGFBP-1( P < 0. 01). Phosphorylations of several downstream signaling molecules including protein kinase B( PKB / Akt),mTOR,and ribosomal protein S6 kinase 1( S6K1) in T / HS group were significantly inhibited as compared with shame group( P <0. 01,P <0. 05,P <0. 05). Muscle 3-MH levels in T/HS rats were also significantly higher than that observed in shame group( P < 0. 01). Conclusion: The derangement of skeletal muscle protein metabolism caused by GH-IGF-1 axis dysfunction may be an important factor leading to the muscle wasting following severe trauma.更多还原