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首页> 外文期刊>Cellular Signalling >Capsaicin exhibits anti-inflammatory property by inhibiting IkB-a degradation in LPS-stimulated peritoneal macrophages
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Capsaicin exhibits anti-inflammatory property by inhibiting IkB-a degradation in LPS-stimulated peritoneal macrophages

机译：辣椒素通过抑制LPS刺激的腹膜巨噬细胞中的IkB-a降解而表现出抗炎特性

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摘要

Capsaicin, a major ingredient of hot pepper, is considered to exhibit an anti-inflammatory property. In order to clarify the signalling mechanism underlying the anti-inflammatory action of capsaicin, we investigated the effect of capsaicin on the production of inflammatory molecules in lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages. The level of PGE2 was measured by EIA. The expression levels of COX-2, iNOS, IkB-a, and vanilloid receptor-1 (VR-1) were determined at the protein and mRNA levels. Significant inhibition of the production of LPS-induced PGE2 by capsaicin was observed in a dose-dependent manner. Capsaicin did not affect the COX-2 expression at either the protein or mRNA level, but inhibited the enzyme activity of COX-2 and the expression of the iNOS protein. Capsaicin completely blocked LPS-induced disappearance of IkB-a and therefore inactivated NF-kB. The inhibitory action of capsaicin on PGE2 production was not abolished by capsazepine, a specific antagonist to VR-1. A high expression level of the VR-1 like protein (VRL-1) was observed in peritoneal macrophages, while the expression of VR-1 was not detected. These findings suggest that the anti-inflammatory action of capsaicin may occur through a novel mechanism, not by a VR-1 receptor-mediated one. Both capsaicin and capsazepine may be a promising drug candidates for ameliorating inflammatory diseases and cancer. (C) 2002 Elsevier Science Inc. All rights reserved. [References: 35]
机译：辣椒素是辣椒的主要成分，被认为具有抗炎特性。为了阐明潜在的辣椒素抗炎作用的信号传导机制，我们研究了辣椒素对脂多糖（LPS）刺激的小鼠腹膜巨噬细胞中炎症分子产生的影响。通过EIA测量PGE 2的水平。在蛋白质和mRNA水平确定了COX-2，iNOS，IkB-a和香草受体-1（VR-1）的表达水平。辣椒素以剂量依赖性方式显着抑制了脂多糖诱导的PGE2的产生。辣椒素在蛋白质或mRNA水平上均不会影响COX-2的表达，但会抑制COX-2的酶活性和iNOS蛋白的表达。辣椒素完全阻断了LPS诱导的IkB-a的消失，从而使NF-kB失活。辣椒素对VR-1的特异性拮抗剂并未消除辣椒素对PGE2产生的抑制作用。在腹膜巨噬细胞中观察到VR-1样蛋白（VRL-1）的高表达水平，而未检测到VR-1的表达。这些发现表明，辣椒素的抗炎作用可能是通过一种新的机制发生的，而不是通过VR-1受体介导的。辣椒素和辣椒素都可能是缓解炎性疾病和癌症的有前途的候选药物。 （C）2002 Elsevier Science Inc.保留所有权利。 [参考：35]

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