Fermented soymilk prevent free fatty acid-induced lipogenesis and production of reactive oxygen species in hepatocellular steatosis model

Abstract

INTRODUCTION: Ingredients of soy and fermented products have been widely utilized as food supplement for health-enhancing properties, such as reducing the risk of osteoporosis, protection of cardiovascular diseases, and prevention of prostate and breast cancer. This study was carried out to examine the effects of fermented soymilk (FSM) on the free fatty acid-induced lipogenesis in an in vitro model of hepatocellular steatosis model. MATERIALS AND METHODS: HepG2 cells were incubated with 0.2 mM of palmitic acid (PA) for 24 h to induce lipogenesis and to accumulate the intracellular lipid accumulation, which was observed by oil red O and Nile red staining. The PA treated cells were co-incubated with 0.04∼1.0% of lyophilized FSM, 0.05 mM of genistein, and 50 nM of estrogen, respectively. Western blot analysis of sterol regulatory element-binding protein-1 (SREBP-1) and nuclear factor erythroid 2-related factor-2 (NRF-2) were performed to examine the lipogenesis related extracellular signal-regulated kinase (ERK) pathway. Cellular reactive oxygen species (ROS) was measured by the DCFDA assay kit. RESULTS: Lipid accumulations in the PA and FSM co-incubated cells were significantly decreased by 0.5% and 1.0% of FSM without cytotoxicity. Treatments of PA and combining with genistein and estrogen significantly increased the expressions of SREBP-1. However, FSM co-incubation significantly attenuated the expression of SREBP-1 in the PA treated 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 1.0% of FSM. Meanwhile, genistein or estrogen alone did not lead to significant differences in ROS production. CONCLUSION: Our results show that bioactive components, except genistein and phytoestrogen, in fermented soymilk protect hepatocytes against lipid accumulation and ROS production induced by free fatty acid. These effects may be mediated by inhibition of SREBP-1 and activation of NFR-2 via ERK pathway in hepatocytes. Disclosures: The following authors have nothing to disclose: Sang Bong Ahn, Byoung Kwan Son, Dae Won Jun, Yong Kyun Cho