Tumour necrosis factor (TNF) and interleukin-1 (IL-1) induce muscle proteolysis through different mechanisms

Oded Zamir, Per Olof Hasselgren, Takashi Higashiguchi, Janice A. Frederick, Josef E. Fischer

研究成果: ジャーナルへの寄稿学術論文査読

44 被引用数 (Scopus)

抄録

The purpose of this study was to test the hypothesis that muscle proteolysis induced by TNF or IL-1 is mediated by glucocorticoids. Rats were treated with 300 μg kg-1 of recombinant human preparations of IL-la (rIL-lα) or TNFα (rTNFα) divided into three equal intraperitoneal doses given over 16 h. Two hours before each cytokine injection, rats were given 5 mg kg1 of the glucocorticoid receptor blocker mifepristone RU 38486, by gavage or were gavaged with the vehicle. Eighteen hours after the first cytokine injection, total and myofibrillar protein breakdown rates were determined in incubated extensor digitorum longus muscles as release of tyrosine and 3- methylhistidine, respectively. Total and myofibrillar proteolytic rates were increased following injection of rIL-lα or rTNFα. Proteolysis induced by rIL-lα was not altered by treatment with RU 38486. In contrast, the glucocorticoid receptor blocker inhibited the proteolytic effect of rTNFα. The results suggest that the proteolytic effect of TNF is mediated by glucocorticoids and that IL-1 induces muscle proteolysis through a glucocorticoid independent pathway.

本文言語英語
ページ(範囲)247-250
ページ数4
ジャーナルMediators of Inflammation
1
4
DOI
出版ステータス出版済み - 1992

All Science Journal Classification (ASJC) codes

  • 免疫学
  • 細胞生物学

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