Garcinia Biflavonoid 1 Improves Lipid Metabolism in HepG2 Cells via Regulating PPARα

• Published in: Molecules (Basel, Switzerland) Vol. 27; no. 6; p. 1978
• Main Authors: Chen, Hai-Xin, Yang, Fan, He, Xin-Qian, Li, Ting, Sun, Yong-Zhi, Song, Jian-Ping, Huang, Xin-An, Guo, Wen-Feng
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 18.03.2022; MDPI
• Subjects: Apoptosis; Biflavonoids - pharmacology; Biological activity; Deposition; fatty acid oxidation; Fatty acids; Fatty liver; Garcinia; garcinia biflavonoid 1; Hep G2 Cells; Humans; Inflammation; Interleukin 1; Interleukin 10; Lipid Metabolism; Lipids; Liver; Liver diseases; Metabolism; Oleic acid; Oxidative metabolism; Oxidative stress; Palmitic acid; PPAR alpha - genetics; PPARα; Triglycerides; Tumor necrosis factor-α; garcinia biflavonoid 1; fatty acid oxidation; PPARα; lipid metabolism
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules27061978

Garcinia biflavonoid 1 (GB1) is one of the active chemical components of and is reported to be capable of reducing the intracellular lipid deposition, which is the most significant characteristic of non-alcoholic fatty liver disease. However, its bioactive mechanism remains elusive. In the current study, the lipid deposition was induced in HepG2 cells by exposure to oleic acid and palmitic acid (OA&PA), then the effect of GB1 on lipid metabolism and oxidative stress and the role of regulating PPARα in these cells was investigated. We found that GB1 could ameliorate the lipid deposition by reducing triglycerides (TGs) and upregulate the expression of PPARα and SIRT6, suppressing the cell apoptosis by reducing the oxidative stress and the inflammatory factors of ROS, IL10, and TNFα. The mechanism study showed that GB1 had bioactivity in a PPARα-dependent manner based on its failing to improve the lipid deposition and oxidative stress in PPARα-deficient cells. The result revealed that GB1 had significant bioactivity on improving the lipid metabolism, and its potential primary action mechanism suggested that GB1 could be a potential candidate for management of non-alcoholic fatty liver disease.