<i>Garcinia cambogia</i> Ameliorates Non-Alcoholic Fatty Liver Disease by Inhibiting Oxidative Stress-Mediated Steatosis and Apoptosis through NRF2-ARE Activation

• Main Authors: Joo-Hui Han (Author), Min-Ho Park (Author), Chang-Seon Myung (Author)
• Format: Book
• Published: MDPI AG, 2021-07-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

Excessive free fatty acids (FFAs) causes reactive oxygen species (ROS) generation and non-alcoholic fatty liver disease (NAFLD) development. <i>Garcinia cambogia</i> (<i>G. cambogia</i>) is used as an anti-obesity supplement, and its protective potential against NAFLD has been investigated. This study aims to present the therapeutic effects of <i>G. cambogia</i> on NAFLD and reveal underlying mechanisms. High-fat diet (HFD)-fed mice were administered <i>G. cambogia</i> for eight weeks, and steatosis, apoptosis, and biochemical parameters were examined in vivo. FFA-induced HepG2 cells were treated with <i>G. cambogia</i>, and lipid accumulation, apoptosis, ROS level, and signal alterations were examined. The results showed that <i>G. cambogia</i> inhibited HFD-induced steatosis and apoptosis and abrogated abnormalities in serum chemistry. <i>G. cambogia</i> increased in NRF2 nuclear expression and activated antioxidant responsive element (ARE), causing induction of antioxidant gene expression. NRF2 activation inhibited FFA-induced ROS production, which suppressed lipogenic transcription factors, C/EBPα and PPARγ. Moreover, the ability of <i>G. cambogia</i> to inhibit ROS production suppressed apoptosis by normalizing the Bcl-2/BAX ratio and PARP cleavage. Lastly, these therapeutic effects of <i>G. cambogia</i> were due to hydroxycitric acid (HCA). These findings provide new insight into the mechanism by which <i>G. cambogia</i> regulates NAFLD progression.

Item Description

10.3390/antiox10081226
2076-3921