首页> 外文期刊>Life sciences >ENDOGENOUS TUMOR NECROSIS FACTOR-ALPHA PRODUCTION BY A PANCREATIC BETA-CELL LINE - INHIBITORY EFFECTS OF HYDROCORTISONE AND NICOTINAMIDE
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ENDOGENOUS TUMOR NECROSIS FACTOR-ALPHA PRODUCTION BY A PANCREATIC BETA-CELL LINE - INHIBITORY EFFECTS OF HYDROCORTISONE AND NICOTINAMIDE

机译:胰β-细胞系生产内源性肿瘤坏死因子-氢化可的松和烟酰胺的抑制作用

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The purpose of this study was to examine regulation of interleukin-1(IL-1)-induced tumor necrosis factor-alpha (TNF-alpha) production by a mouse beta-cell line (beta TC1). Three-hour incubation of beta TC1 cells with 5 U/ml of IL-1 beta results in the expression of TNF-alpha mRNA and intracellular accumulation of TNF-alpha. It has been shown that glucocorticoids and immunosuppressive agents such as cyclosporin and FK-506 inhibit TNF-alpha generation by T-lymphocytes and monocytes. Hydrocortisone of 1 and 10 mu mol/l suppressed TNF-alpha mRNA levels and the TNF-alpha content of beta TC1 cells exposed to IL-1 beta, whereas neither cyclosporin nor FK-506 altered the TNF-alpha content. Nicotinamide of 5-10 mmol/l also reduced TNF-alpha mRNA and TNF-alpha protein levels in beta TC1 cells. Addition of exogenous TNF-alpha did not inhibit IL-1-induced transcription of TNF-alpha gene. These observations support the potential therapeutic role of glucocorticoids and nicotinamide in protecting beta-cells against cytokine-mediated damage, although glucocorticoid agonists have hyperglycemic metabolic effects. [References: 29]
机译:这项研究的目的是检查小鼠白细胞(βTC1)对白介素-1(IL-1)诱导的肿瘤坏死因子-α(TNF-α)产生的调节。 βTC1细胞与5 U / ml的IL-1β孵育3小时会导致TNF-αmRNA的表达和TNF-α的细胞内积累。已经显示,糖皮质激素和免疫抑制剂如环孢菌素和FK-506抑制T淋巴细胞和单核细胞产生TNF-α。 1和10μmol/ l的氢化可的松抑制暴露于IL-1β的βTC1细胞的TNF-αmRNA水平和TNF-α含量,而环孢菌素和FK-506均未改变TNF-α含量。 5-10 mmol / l的烟酰胺还可以降低βTC1细胞中的TNF-αmRNA和TNF-α蛋白水平。外源TNF-α的添加不会抑制IL-1诱导的TNF-α基因的转录。这些观察结果支持糖皮质激素和烟酰胺在保护β细胞免受细胞因子介导的损害中的潜在治疗作用,尽管糖皮质激素激动剂具有高血糖代谢作用。 [参考:29]

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