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ameliorates non-alcoholic fatty liver disease by inhibiting oxidative stress-mediated steatosis and apoptosis through NRF2-ARE activation
Joo-Hui Han, Min-Ho Park, Chang-Seon Myung
Excessive free fatty acids (FFAs) causes reactive oxygen species (ROS) generation and non-alcoholic fatty liver disease (NAFLD) development.
) 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
on NAFLD and reveal underlying mechanisms. High-fat diet (HFD)-fed mice were administered
for eight weeks, and steatosis, apoptosis, and biochemical parameters were examined in vivo. FFA-induced HepG2 cells were treated with
, and lipid accumulation, apoptosis, ROS level, and signal alterations were examined. The results showed that
inhibited HFD-induced steatosis and apoptosis and abrogated abnormalities in serum chemistry.
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
to inhibit ROS production suppressed apoptosis by normalizing the Bcl-2/BAX ratio and PARP cleavage. Lastly, these therapeutic effects of
were due to hydroxycitric acid (HCA). These findings provide new insight into the mechanism by which
regulates NAFLD progression.
; non-alcoholic fatty liver disease (NAFLD); steatosis; apoptosis; reactive oxygen species; antioxidant; NRF2; hydroxycitric acid
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