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脓毒症时肌分解代谢旺盛,外周释放氨基酸,肝摄取氨基酸和急性相蛋白合成加快,这一过程由细胞素引起。实验证明,细胞素和糖皮质类固醇是“肝-骨骼肌轴心”的两个重要介质。IL-1、IL-6和TNF直接调节肝细胞的蛋白合成,而糖皮质类固醇则是辅助因子。肌蛋白分解由糖皮质类固醇中介或需它参加,但阻断糖皮质类固醇受体并不能完全阻断脓毒症引起的这种反应,提示除糖皮质类固醇外,其它细胞素特别是TNF刺激糖皮质类固醇释放,并在细胞水平与它相互作用,从而引起肌蛋白分解代谢,但IL-1引起的肌蛋白分解可能不经糖皮质类固醇介导。
Sepsis strong muscle catabolism, peripheral release of amino acids, liver amino acids and acute phase protein synthesis speed up, this process is caused by cytokines. Experiments show that cytokines and glucocorticoid are “liver - skeletal axis” of the two important mediators. IL-1, IL-6 and TNF directly regulate protein synthesis in liver cells, whereas glucocorticosteroids are cofactors. Muscle proteolysis is mediated or required by glucocorticosteroid blockade, but blockade of glucocorticosteroid receptors does not completely block this response caused by sepsis, suggesting that other cytokines, particularly TNF-stimulated sugars, in addition to glucocorticoid Corticosteroids release and interact with it at the cellular level, causing muscle catabolism, but the IL-1-induced muscle proteolysis may not be mediated by glucocorticosteroids.