Raphani Semen (Raphanus sativus L.) Ameliorates Alcoholic Fatty Liver Disease by Regulating De Novo Lipogenesis.

Woo Yong Park,Taegon Kim,Jae Jin Kim,Seokbeom Hong,Jinbong Park,Joon Hak Noh,Gahee Song,Jae-Young Um

doi:10.3390/nu13124448

Abstract

In this study, we investigated the pharmacological effect of a water extract of Raphani Semen (RSWE) on alcoholic fatty liver disease (AFLD) using ethanol-induced AFLD mice (the NIAAA model) and palmitic acid (PA)-induced steatosis HepG2 cells. An RSWE supplement improved serum and hepatic triglyceride (TG) levels of AFLD mice, as well as their liver histological structure. To explore the molecular action of RSWE in the improvement of AFLD, we investigated the effect of RSWE on four major pathways for lipid homeostasis in the liver: free fatty acid transport, lipogenesis, lipolysis, and β-oxidation. Importantly, RSWE decreased the mRNA expression of de novo lipogenesis-related genes, such as Srebf1, Cebpa, Pparg, and Lpin1, as well as the protein levels of these factors, in the liver of AFLD mice. That these actions of RSWE affect lipogenesis was confirmed using PA-induced steatosis HepG2 cells. Overall, our findings suggest that RSWE has the potential for improvement of AFLD by inhibiting de novo lipogenesis.

Highlights

Alcoholic fatty liver disease (AFLD), characterized by excessive fortification of triglycerides in the liver, is one of the major causes of the wide spectrum of hepatic pathologies, such as hepatitis, steatohepatitis, fibrosis cirrhosis, and hepatocellular carcinoma (HCC) [1]
The mice were randomly divided into three groups of four mice each, as follows: liquid diet (LD) group (LD-fed), AFLD group (ELD and 35% EtOH-fed), and RSWE group (ELD and 35% EtOH-fed with RSWE 100 mg/kg, per oral)
Body weights and liver weights of the AFLD group were significantly decreased compared to the LD group, but RSWE treatment had no effect on the reduced body and liver weights (Figure 1B)

Summary

Introduction

Alcoholic fatty liver disease (AFLD), characterized by excessive fortification of triglycerides in the liver, is one of the major causes of the wide spectrum of hepatic pathologies, such as hepatitis, steatohepatitis, fibrosis cirrhosis, and hepatocellular carcinoma (HCC) [1]. Lipid homeostasis in the liver is maintained by regulating de novo lipogenesis, oxidation, and transport of fatty acids. Fatty acids are either oxidized by mitochondrial β-oxidation or incorporated into TG, resulting in lipid accumulation in the liver [6]. Many factors mediate lipid homeostasis in the liver by regulating de novo lipogenesis, oxidation, and transport of fatty acids. Given that hepatocellular lipid accumulation is the earliest sign of alcoholic liver disease, further study on the regulation of lipid metabolism in hepatocytes could create opportunities for early therapeutic intervention for those at risk of advanced disease [4]

Methods

Results

Conclusion