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地塞米松抑制肿瘤坏死因子的细胞毒性活性。

Dexamethasone inhibits the cytotoxic activity of tumor necrosis factor.

作者信息

Tsujimoto M, Okamura N, Adachi H

机构信息

Suntory Institute for Biomedical Research, Osaka, Japan.

出版信息

Biochem Biophys Res Commun. 1988 May 31;153(1):109-15. doi: 10.1016/s0006-291x(88)81196-3.

Abstract

Effect of dexamethasone (DEX) on the cytotoxic activity of tumor necrosis factor (TNF) was examined using murine fibroblast cell line (L929 cells). DEX protected cells from the cytotoxic action of TNF. Protection of cytotoxic action was apparent when cells were pre-treated with DEX for 12h and no protection was observed in the presence of cycloheximide. These results suggested that de novo synthesis of new proteins was required for DEX-mediated protection. Moreover, prolonged simultaneous treatment with TNF and DEX resulted in the enhancement of cell growth, suggesting that TNF acted as a growth factor when cells were protected from the cytotoxic action of TNF. These results suggested that the signal transduction system for fibroblast growth enhancing and cytotoxic action of TNF were different from each other and that the interaction between TNF and glucocorticoids may play a modulating role in some inflammatory processes in vivo.

摘要

使用小鼠成纤维细胞系(L929细胞)检测了地塞米松(DEX)对肿瘤坏死因子(TNF)细胞毒性活性的影响。DEX保护细胞免受TNF的细胞毒性作用。当细胞用DEX预处理12小时时,细胞毒性作用的保护作用明显,而在存在环己酰亚胺的情况下未观察到保护作用。这些结果表明,DEX介导的保护作用需要新蛋白质的从头合成。此外,TNF和DEX的长期同时处理导致细胞生长增强,这表明当细胞免受TNF的细胞毒性作用时,TNF起生长因子的作用。这些结果表明,TNF促进成纤维细胞生长和细胞毒性作用的信号转导系统彼此不同,并且TNF与糖皮质激素之间的相互作用可能在体内某些炎症过程中起调节作用。

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