Regulation of peptide-chain initiation in muscle during sepsis by interleukin-1 receptor antagonist.
Regulation of peptide-chain initiation in muscle during sepsis by interleukin-1 receptor antagonist.
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白介素 1 受体拮抗剂对脓毒症期间肌肉中肽链起始的调节。
DOI：
10.1152/ajpendo.1996.271.3.e513
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Cooney,RN
中科院分区：
文献类型：
--
作者：
Vary,TC;Voisin,L;Cooney,RN
探讨白细胞介素1(IL-1)对高代谢脓毒症大鼠骨骼肌蛋白质合成的调节机制。用白介素1受体拮抗剂(IL-1ra)治疗脓毒症大鼠，可阻止脓毒症引起的腓肠肌蛋白质合成和翻译效率的抑制。核糖体亚基分析显示，在脓毒症大鼠中观察到的40S和60S核糖体游离亚基的增加被IL-1ra阻止，这表明多肽链的起始维持在控制值。在输注IL-1ra后，脓毒症未能抑制肽链的启动，这与真核细胞启动因子(EIF)2B的epsilon亚单位(eIF-2B epsilon)蛋白维持在控制值有关。IL-1ra处理前后脓毒症大鼠腓肠肌eIF-2B epsilon蛋白含量的变化与eIF-2B epsilon mRNA丰度的变化相关。结果表明，IL-1ra可抑制脓毒症时蛋白合成的抑制和抑制EIF-2B的表达，从而减轻脓毒症所致的蛋白质合成抑制。
The mechanism by which interleukin-1 (IL-1) regulates protein synthesis in skeletal muscle during hypermetabolic sepsis in rats was investigated. Treatment of septic rats with a specific interleukin-1 receptor antagonist (IL-1ra) prevented the sepsis-induced inhibition of protein synthesis and translational efficiency in gastrocnemius. Analysis of ribosomal subunits revealed that the increase in free 40S and 60S ribosomal subunits observed in septic rats was prevented by infusion of IL-1ra, indicating peptide-chain initiation was maintained at control values. The failure of sepsis to inhibit peptide-chain initiation after infusion of IL-1ra correlated with a maintenance of the epsilon-subunit of eukaryotic initiation factor (eIF) 2B (eIF-2B epsilon) protein at control values. The alterations in the eIF-2B epsilon protein content in gastrocnemius of septic rats treated with or without IL-1ra were associated with corresponding changes in the abundance of eIF 2B epsilon mRNA. The results provide evidence that infusion of IL-1ra attenuates the sepsis-induced inhibition of protein synthesis by preventing the inhibition of peptide-chain initiation and downregulation of eIF-2B expression during sepsis.