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    Online Resource
    Online Resource
    SAGE Publications ; 2014
    In:  Experimental Biology and Medicine Vol. 239, No. 3 ( 2014-03), p. 284-292
    In: Experimental Biology and Medicine, SAGE Publications, Vol. 239, No. 3 ( 2014-03), p. 284-292
    Abstract: Oleanolic acid is a pentacyclic triterpenoid naturally present in foods and medicinal plants with anticancer, antioxidant, and antiaging properties. The current study elucidated that oleanolic acid inhibited the production of insulin-mimetic and inflammatory adipokine of visfatin during adipogenic differentiation of 3T3-L1 adipocytes. Adipocytes were cultured in an adipogenic media with and without 1–25 µM oleanolic acid up to 8 days for differentiation. The cellular expression and secretion of visfatin was markedly enhanced in differentiating adipocytes, which was dose-dependently attenuated by 1–25 µM oleanolic acid. Secretion of interleukin (IL)-6 and macrophage inflammatory protein (MIP)-2 was highly elevated during differentiation, which was much earlier than visfatin production of adipocytes. The visfatin production was secondary to inflammatory IL-6 and MIP-2. This study further elucidated that nuclear factor-κB (NF-κB) signaling was responsible for cellular production of visfatin. NF-κB was activated by translocating into the nucleus with increased phosphorylation of inhibitory κB (IκB), which was disturbed by oleanolic acid. Cellular expression of tumor necrosis factor receptor associated factor 6 (TRAF6), a NF-κB upstream, was upregulated in parallel with transactivation with NF-κB. The TRAF6 induction required the auto-stimulation of inflammatory IL-6 and MIP-2. These results demonstrate that oleanolic acid inhibited visfatin and its inflammatory response during adipocyte differentiation through blocking IL-6-TRAF6-NF-κB signaling. Therefore, oleanolic acid may be a potent therapeutic agent targeting against adipogenesis and visfatin-linked inflammation.
    Type of Medium: Online Resource
    ISSN: 1535-3702 , 1535-3699
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2014
    detail.hit.zdb_id: 2020856-X
    SSG: 12
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