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Fermented Soymilk Alleviates Lipid Accumulation by Inhibition of SREBP-1 and Activation of NRF-2 in the Hepatocellular Steatosis Model

Authors
Ahn, Sang BongWu, Wen HaoLee, Jong HunJun, Dae WonKim, JihyunKim, RijiLee, Tae-bokJun, Jin Hyun
Issue Date
Feb-2018
Publisher
KOREAN SOC MICROBIOLOGY & BIOTECHNOLOGY
Keywords
Fermented soymilk; steatosis model; HepG2; SREBP-1; NRF-2
Citation
Journal of Microbiology and Biotechnology, v.28, no.2, pp.236 - 245
Indexed
SCIE
SCOPUS
KCI
Journal Title
Journal of Microbiology and Biotechnology
Volume
28
Number
2
Start Page
236
End Page
245
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/17801
DOI
10.4014/jmb.1707.07061
ISSN
1017-7825
Abstract
Ingredients of soy and fermented soy products have been widely utilized as food supplements for health-enhancing properties. The aim of this study was to evaluate the effects of fermented soymilk (FSM) and soymilk (SM) on free fatty acid-induced lipogenesis in the hepatocellular steatosis model. HepG2 cells were incubated with palmitic acid (PA) for 24 h to induce lipogenesis and accumulation of intracellular lipid contents. The PA-treated cells were co-incubated with FSM, SM, genistein, and estrogen, respectively. Lipid accumulation in the PA-treated HpG2 cells was significantly decreased by co-incubation with FSM. Treatment of HepG2 cells with PA combined with genistein or estrogen significantly increased the expression of SREBP-1. However, FSM co-incubation significantly attenuated SREBP-1 expression in the PA-treated HepG2 cells; in addition, expression of NRF-2 and phosphorylation of ERK were significantly increased in the PA and FSM co-incubated cells. PA-induced ROS production was significantly reduced by FSM and SM. Our results suggested that the bioactive components of FSM could protect hepatocytes against the lipid accumulation and ROS production induced by free fatty acids. These effects may be mediated by the inhibition of SREBP-1 and the activation of NRF-2 via the ERK pathway in HepG2 cells.
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