姜黄素不是过氧化物酶体增殖物激活受体-γ的配体

Gene Therapy and Molecular Biology Pub Date : 2009-04-01
Venkata R Narala, Monica R Smith, Ravi K Adapala, Rajesh Ranga, Kalpana Panati, Bethany B Moore, Todd Leff, Vudem D Reddy, Anand K Kondapi, Raju C Reddy
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引用次数: 0

摘要

姜黄素,一种在香料姜黄中发现的化合物,已被证明具有通过各种不同机制发挥的许多有益的生物活性。据报道,姜黄素的一些作用涉及核转录因子过氧化物酶体增殖物激活受体-γ (PPAR-γ)的激活,但姜黄素可能是PPAR-γ配体的概念仍然存在争议。本文报道的结果表明,与PPAR-γ配体西格列酮和罗格列酮不同,姜黄素在五种不同的报告基因或dna结合试验中均无活性,不会取代[(3)H]罗格列酮与PPAR-γ配体结合位点,不会诱导PPAR-γ依赖性前脂肪细胞分化,而其抑制成纤维细胞向肌成纤维细胞分化的能力不受四种PPAR-γ拮抗剂的影响。这些多重证据最终表明姜黄素不是PPAR-γ配体,并表明需要进一步研究该化合物的作用机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Curcumin is not a ligand for peroxisome proliferator-activated receptor-γ

Curcumin, a compound found in the spice turmeric, has been shown to possess a number of beneficial biological activities exerted through a variety of different mechanisms. Some curcumin effects have been reported to involve activation of the nuclear transcription factor peroxisome proliferator-activated receptor-γ (PPAR-γ), but the concept that curcumin might be a PPAR-γ ligand remains controversial. Results reported here demonstrate that, in contrast to the PPAR-γ ligands ciglitazone and rosiglitazone, curcumin is inactive in five different reporter or DNA-binding assays, does not displace [(3)H]rosiglitazone from the PPAR-γ ligand-binding site, and does not induce PPAR-γ-dependent differentiation of preadipocytes, while its ability to inhibit fibroblast-to-myofibroblast differentiation is not affected by any of four PPAR-γ antagonists. These multiple lines of evidence conclusively demonstrate that curcumin is not a PPAR-γ ligand and indicate the need for further investigation of the mechanisms through which the compound acts.

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Gene Therapy and Molecular Biology
Gene Therapy and Molecular Biology 生物-生化与分子生物学
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