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Red ginseng-derived saponin fraction suppresses the obesity-induced inflammatory responses via Nrf2-HO-1 pathway in adipocyte-macrophage co-culture system

Authors
Kim, Chae YoungKang, BobinSuh, Hyung JooChoi, Hyeon-Son
Issue Date
12월-2018
Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
Keywords
Obesity-induced inflammation; Co-culture; Saponin fraction; Nuclear factor (erythroid-derived 2)-like 2; (Nrf2)-hemoxygenase-1 (HO-1) signaling pathway
Citation
BIOMEDICINE & PHARMACOTHERAPY, v.108, pp.1507 - 1516
Indexed
SCIE
SCOPUS
Journal Title
BIOMEDICINE & PHARMACOTHERAPY
Volume
108
Start Page
1507
End Page
1516
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/71451
DOI
10.1016/j.biopha.2018.09.169
ISSN
0753-3322
Abstract
The aim of this study was to investigate the effect of saponin fraction (SF) from red ginseng on obesity-induced inflammatory response in a co-culture system of 3T3-L1 and RAW264.7 cells. HPLC analysis showed that SF contains more than 50% ginsenosides, and Rb1 was the most abundant ginsenoside [135.31 mu g/mg (extract)]. The production of nitric oxide and cytokines, induced by adipocyte-conditioned medium (3T3-CM), was significantly decreased by SF. SF (100 mu g/mL) suppressed the abundance of tumor necrosis factor-alpha (TNF-alpha), monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 (IL-6) by 78%, 40%, and 22%, respectively. This SF-mediated reduction in inflammatory cytokines was due to the suppression of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (I kappa B alpha) phosphorylation, and translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B) into the nucleus. SF also regulated adipokine expression in adipocytes, which were stimulated by macrophage-conditioned medium (RAW-CM); adiponectin expression was upregulated (> 2-fold), while resistin was downregulated (40%). In the contact system of adipocytes and macrophages, SF significantly decreases MCP-1 (37%) and IL-6 (25%) production. In the transwell system, SF (100 mu g/mL) significantly increased the abundance of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and its target protein, hemoxygenase-1 (HO-1) by 1.5 similar to 3.5-fold and 2.8 similar to 3.6-fold, respectively, thus increasing Nrf2 translocation into nucleus. However, SF-mediated inhibitory effect on the release of IL-6 and MCP-1 cytokines was reversed in the Nrf2 or HO-1 knockdown condition. This result indicated that SF-mediated inhibition of obesity-induced inflammation was dependent on Nrf2 activation.
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Suh, Hyung Joo
보건과학대학 (바이오시스템의과학부)
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