Abstract
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease found worldwide. The present study aimed to evaluate the mechanisms of inhibiting lipid accumulation in free fatty acid (FFA)-treated HepG2 cells caused by bark and fruit extracts of Toona sinensis (TSB and TSF). FFA induced lipid and triglyceride (TG) accumulation, which was attenuated by TSB and TSF. TSB and/or TSF promoted phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-coA carboxylase and peroxisome proliferator-activated receptor alpha upregulation. Furthermore, TSB and TSF suppressed FFA-induced liver X receptor, sterol regulatory element-binding transcription protein 1, fatty acid synthase, and stearoyl-CoA desaturase 1 protein expression. Moreover, TSB and/or TSF induced phosphorylation of Unc-51 like autophagy-activating kinase and microtubule-associated protein 1A/1B-light chain 3 expressions. Therefore, TSB and TSF relieve lipid accumulation by attenuating lipogenic protein expression, activating the AMPK pathway, and upregulating the autophagic flux to enhance lipid metabolism. Moreover, TSB and TSF reduced TG contents, implying the therapeutic use of TSB and TSF in NAFLD.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a global health issue driven by dysregulation of lipid homeostasis [1]
The present study investigated the molecular mechanism of the effects of TSB and T. sinensis fruit (TSF) extracts on lipid accumulation using an in vitro cellular model
T. sinensis is a popular dish in Asia and Taiwan, and vegetarians use it as flavoring
Summary
Non-alcoholic fatty liver disease (NAFLD) is a global health issue driven by dysregulation of lipid homeostasis [1]. Emerging evidence suggests that AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor alpha (PPARα) and LC3 are critical regulators of hepatic lipid metabolism and could be therapeutic targets in NAFLD [10]. These target proteins exhibit interactions; for example, phosphorylation of Thr172 in the α-subunit of AMPK activates acetyl-coA carboxylase (ACC)-SREBP-1c, PPARα, and Unc-51-like autophagy activating kinase (ULK1)-LC3 [11,12]. The present study investigated the molecular mechanism of the effects of TSB and TSF extracts on lipid accumulation using an in vitro cellular model
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