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肿瘤坏死因子(TNF)在人肝细胞原代培养物中可抑制白细胞介素(IL)-1和/或IL-6刺激的C反应蛋白(CRP)及血清淀粉样蛋白A(SAA)的合成。

Tumor necrosis factor (TNF) inhibits interleukin (IL)-1 and/or IL-6 stimulated synthesis of C-reactive protein (CRP) and serum amyloid A (SAA) in primary cultures of human hepatocytes.

作者信息

Yap S H, Moshage H J, Hazenberg B P, Roelofs H M, Bijzet J, Limburg P C, Aarden L A, van Rijswijk M H

机构信息

Division of Liver and Pancreatic Diseases, University Hospital Gasthuisberg, Leuven, Belgium.

出版信息

Biochim Biophys Acta. 1991 Feb 19;1091(3):405-8. doi: 10.1016/0167-4889(91)90207-e.

Abstract

Interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF) are considered as important mediators for the modulation of liver synthesis of acute phase proteins. However, studies of the direct effect of individual or a combination of these cytokines on the synthesis of acute phase proteins in human hepatocytes are still very limited. In this study, we have examined the synthesis of C-reactive protein (CRP) and serum amyloid A (SAA) in primary cultures of human hepatocytes exposed to recombinant(r)IL-1 alpha (100 U/ml), rIL-6 (2000 U/ml), rTNF alpha (30 U/ml) and to various combinations of these cytokines in the presence of 1 microM dexamethasone. Monoclonal antibodies to rTNF alpha and monospecific anti-rIL-6 sheep antiserum were also used to investigate the possible endogenous production of TNF or IL-6. The findings indicate: (1) IL-1 and IL-6 are stimulatory cytokines for the liver synthesis of CRP and SAA. Anti IL-6 abolishes the stimulatory effect of IL-1. These findings support the previous observation and indicate that IL-1 exerts its action on the enhanced synthesis of CRP and SAA at least in part via IL-6 production in the liver cell. (2) TNF is an inhibitory cytokine for the liver synthesis of CRP. It inhibits also the stimulatory effect of IL-1 and IL-6 on the synthesis of CRP and SAA. (3) Since anti-TNF enhances the stimulatory effect of IL-6 on the synthesis of CRP and SAA, it seems likely that TNF is also produced by the human hepatocytes. However, further studies for more direct evidence of the liver cell production of TNF, such as the detection of TNF messenger RNA are required.

摘要

白细胞介素(IL)-1、IL-6和肿瘤坏死因子(TNF)被认为是调节肝脏急性期蛋白合成的重要介质。然而,关于这些细胞因子单独或联合作用对人肝细胞急性期蛋白合成的直接影响的研究仍然非常有限。在本研究中,我们检测了在1 microM地塞米松存在的情况下,重组(r)IL-1α(100 U/ml)、rIL-6(2000 U/ml)、rTNFα(30 U/ml)以及这些细胞因子的各种组合作用下人原代肝细胞中C反应蛋白(CRP)和血清淀粉样蛋白A(SAA)的合成。还使用了抗rTNFα单克隆抗体和单特异性抗rIL-6羊抗血清来研究TNF或IL-6可能的内源性产生。研究结果表明:(1)IL-1和IL-6是肝脏合成CRP和SAA的刺激细胞因子。抗IL-6可消除IL-1的刺激作用。这些结果支持了先前的观察,并表明IL-1至少部分通过肝细胞中IL-6的产生对CRP和SAA合成的增强发挥作用。(2)TNF是肝脏合成CRP的抑制细胞因子。它也抑制IL-1和IL-6对CRP和SAA合成的刺激作用。(3)由于抗TNF增强了IL-6对CRP和SAA合成的刺激作用,人肝细胞似乎也产生TNF。然而,需要进一步研究以获得肝细胞产生TNF的更直接证据,例如检测TNF信使核糖核酸。

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