Abstract

As one of the wide‐ranging form of chronic liver disease, there are only limited therapeutic options for nonalcoholic fatty liver disease (NAFLD). We evaluated whether fermented black radish (Raphanus sativus L. var. niger; FBR) ameliorates lipid accumulation, inflammation, and hepatic fibrosis, which are characteristics of the pathogenesis of NAFLD. Fermented black radish treatment reduced lipid accumulation in 3T3‐L1 adipocytes, which appeared to be associated with the downregulation of adipogenic transcription factors, including sterol regulatory element‐binding protein 1c, CCAAT/enhancer‐binding protein α, peroxisome proliferator‐activated receptor γ, and lipid accumulation‐related genes including adipocyte protein‐2 and fatty acid synthase. Administration of FBR to C57BL/6J mice challenged with methionine and choline deficient (MCD) diet significantly attenuated the increased serum levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and triglyceride. In addition, treatment with FBR interestingly repressed the hepatic inflammation induced with MCD diet, by lowering the expression of inducible nitric oxide synthase and suppressing the inactivation of macrophages and Kupffer cells in the liver. Fermented black radish was also shown to mitigate liver fibrosis through the inhibition of alpha‐smooth muscle actin, transforming growth factor beta‐1, and collagen type I alpha 1 chain. Our results indicate that FBR ameliorates NAFLD and its related metabolic disease by regulating multiple pathways, suggesting that FBR may be an effective dietary supplement for ameliorating NAFLD.

Highlights

  • Nonalcoholic fatty liver disease (NAFLD) is a clinical‐pathological syndrome that is described as fatty infiltration of the liver exceeding5%–10% by weight

  • Our results showed that fermented black radish (FBR) attenuated adipocyte differentiation and lipid accumulation in 3T3‐L1 preadipocytes and suppressed key regulators of hepatic steatosis, inflammation, and fibrosis in the livers of animal model

  • Regarding the mechanism of the hepatoprotective effects of FBR, we postulate that FBR‐induced reductions in lipid accumulation and TG content in 3T3‐L1 cells are related to the reduction in adipogenic transcription factors and the expression of genes related to lipid accumulation

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Summary

Introduction

Nonalcoholic fatty liver disease (NAFLD) is a clinical‐pathological syndrome that is described as fatty infiltration of the liver exceeding5%–10% by weight. Choline and methionine are two essential nutrient components deficiency of which impede beta‐oxidation and synthesis of very low‐density lipoprotein (VLDL) particles (Ibrahim, Hirsova, Malhi, & Gores, 2016). The MCD diet‐induced model of liver injury is characterized by elevated triglyceride (TG) and free fatty acid levels in the liver, as well as lowered serum TG levels (Lee et al, 2018). Hepatocellular damage in this model as described with histopathology include hepatocyte ballooning and cell death, along with infiltration of inflammatory cells or varying degrees of fibrosis (Yeh & Brunt, 2014)

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