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Ursolic acid enhances nitric oxide and tumor necrosis factor‐α production via nuclear factor‐κB activation in the resting macrophages
Author(s) -
You Ho Jin,
Choi Chul Yung,
Kim Ji Young,
Park Sung Jun,
Hahm Kyung-Soo,
Jeong Hye Gwang
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)03161-1
Subject(s) - nitric oxide , tumor necrosis factor alpha , transactivation , nitric oxide synthase , chemistry , ursolic acid , proinflammatory cytokine , downregulation and upregulation , electrophoretic mobility shift assay , transcription factor , microbiology and biotechnology , nf κb , biochemistry , biology , endocrinology , signal transduction , immunology , inflammation , gene , organic chemistry , chromatography
Ursolic acid (UA), a pentacyclic triterpene acid, is reported to have anti‐tumor activities; however, the mechanism underlying its anti‐tumorigenic effects is poorly understood. To further determine the mechanism of UA, we investigated the effects of UA on the release of nitric oxide (NO) and tumor necrosis factor‐α (TNF‐α), and on the level of inducible nitric oxide synthase (iNOS) and TNF‐α gene expression in mouse resting macrophages. We found that UA elicited a dose‐dependent increase in NO and TNF‐α production, and the level of iNOS and TNF‐α mRNA. Transient expression and electrophoretic mobility shift assays with nuclear factor‐κB (NF‐κB) binding sites revealed that the increased level of iNOS mRNA and TNF‐α mRNA induced by UA were mediated by the NF‐κB transcription factor complex. These results demonstrate that UA stimulates NO and TNF‐α release and is able to upregulate iNOS and TNF‐α expression through NF‐κB transactivation in the resting macrophages.