Increased intestinal protein synthesis during sepsis and following the administration of tumour necrosis factor alpha or interleukin-1 alpha.

Increased intestinal protein synthesis during sepsis and following the administration of tumour necrosis factor alpha or interleukin-1 alpha.
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脓毒症期间以及施用肿瘤坏死因子 α 或白细胞介素 1 α 后肠道蛋白质合成增加。

DOI:
10.1042/bj2860585
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发表时间:
1992
期刊:
The Biochemical journal
影响因子:
--
通讯作者:
Fischer,JE
Fischer,JE
中科院分区:
--
文献类型:
--
作者:
vonAllmen,D;Hasselgren,PO;Higashiguchi,T;Frederick,J;Zamir,O;Fischer,JE

文献摘要

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研究了脓毒症对大鼠肠道蛋白合成的影响。盲肠结扎穿刺(CLP)致脓毒症;对对照大鼠进行假手术。在大量注射[14C]亮氨酸后,测定了空肠和回肠的体内蛋白质合成。在CLP后8小时,蛋白质合成率增加了大约。在空肠黏膜中添加15%,CLP后16 h,空肠和回肠黏膜和血清肌层的蛋白质合成率均提高了50-60%。在第二组实验中,给大鼠注射重组肿瘤坏死因子α (rTNF α)或重组白细胞介素-1 α (il -1 α),总剂量为300微克/千克体重,持续16小时。对照组大鼠给予相应体积的溶剂。用rTNF α治疗导致大约。空肠黏膜蛋白合成增加25%。用il -1 α治疗后,空肠黏膜的蛋白质合成增加了25%,回肠黏膜的蛋白质合成几乎增加了一倍。结果表明,脓毒症刺激肠道蛋白合成,这种反应可能,至少部分是由TNF和/或IL-1介导的。
The influence of sepsis on intestinal protein synthesis was studied in rats. Sepsis was induced by caecal ligation and puncture (CLP); control rats were sham-operated. Protein synthesis was measured in vivo in the jejunum and ileum following a flooding dose of [14C]leucine. At 8 h after CLP the protein synthesis rate was increased by approx. 15% in jejunal mucosa, and at 16 h after CLP, the protein synthesis rate was increased by 50-60% in the mucosa and seromuscular layer of both jejunum and ileum. In a second series of experiments, rats were treated with recombinant tumour necrosis factor alpha (rTNF alpha) or recombinant interleukin-1 alpha (rIL-1 alpha) administered at a total dose of 300 micrograms/kg body weight over 16 h. Control rats received corresponding volumes of solvent. Treatment with rTNF alpha resulted in an approx. 25% increase in mucosal protein synthesis in jejunum. Following treatment with rIL-1 alpha, protein synthesis increased by 25% in jejunal mucosa and almost doubled in ileal mucosa. The results suggest that sepsis stimulates intestinal protein synthesis and that this response may, at least in part, be mediated by TNF and/or IL-1.