Platycodi Radix Extract Prevents Hepatic Steatosis by Enhancing Bile Acid Synthesis in a High-Fat Diet-Induced Fatty Liver Mouse Model

• Published in: Nutrients Vol. 16; no. 6; p. 893
• Main Authors: Kim, Wooyoung, Baek, Woon Hee, Yun, Sung Ho, Lee, Hayoung, Kim, Mi Jeong, Lee, Sang-Yeop, Kim, Gun-Hwa, Kim, Seung Il, Jeong, Hye Gwang, Park, Edmond Changkyun
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 20.03.2024; MDPI
• Subjects: cholesterol; Diabetes; Diet; Fatty acids; Glucose; Insulin resistance; Laboratory animals; Lipids; Liver diseases; Metabolism; Natural products; non-alcoholic fatty liver disease (NAFLD); Obesity; Oxidation; Peptides; Platycodi Radix; Platycodon grandiflorum; Proteins; proteomics; Software; United Kingdom > UK; United States > US; non-alcoholic fatty liver disease (NAFLD); proteomics; bile acid; cholesterol; Platycodi Radix; obesity; Platycodon grandiflorum
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu16060893

We aimed to identify the mechanism underlying the preventive effects of non-alcoholic fatty liver disease (NAFLD) through consumption using liver proteomic and bioinformatic analysis. C57BL/6J mice were categorized into three groups: those receiving a standard chow diet (NCD), those on a high-fat diet (HFD), and those on an HFD supplemented with 5% extract (PRE). After a 12-week period, PRE-fed mice exhibited a noteworthy prevention of hepatic steatosis. Protein identification and quantification in liver samples were conducted using LC-MS/MS. The identified proteins were analyzed through Ingenuity Pathway Analysis software, revealing a decrease in proteins associated with FXR/RXR activation and a concurrent increase in cholesterol biosynthesis proteins in the PRE-treated mouse liver. Subsequent network analysis predicted enhanced bile acid synthesis from these proteins. Indeed, the quantity of bile acids, which was reduced in HFD conditions, increased in the PRE group, accompanied by an elevation in the expression of synthesis-related proteins. Our findings suggest that the beneficial effects of PRE in preventing hepatic steatosis may be mediated, at least in part, through the modulation of FXR/RXR activation, cholesterol biosynthesis, and bile acid synthesis pathways.