4.7 Article

β-patchoulene improves lipid metabolism to alleviate non-alcoholic fatty liver disease via activating AMPK signaling pathway

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 134, Issue -, Pages -

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2020.111104

Keywords

beta-Patchoulene; Pogostemon cablin; Non-alcoholic fatty liver disease; Hepatic steatosis; AMP-activated protein kinase

Funding

  1. Guangdong Basic and Applied Basic Research Foundation [2019A1515110394]
  2. Special Project on the Integration of Industry, Education and Research of Guangdong Province [2014B090902002]
  3. Key Program for Subject Research of Guangzhou University of Chinese Medicine [XK2019002]
  4. Characteristic Cultivation Program for Subject Research of Guangzhou University of Chinese Medicine [XKP2019007]

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This study investigated the effect and potential mechanism of beta-patchoulene (beta-PAE) on non-alcoholic fatty liver disease (NAFLD). The results demonstrated that beta-PAE significantly reduced hepatic steatosis induced by high fat diet and free fatty acids, by regulating AMPK signaling pathway to modulate hepatic lipid synthesis and oxidation.
Non-alcoholic fatty liver disease (NAFLD) has been a leading cause of chronic metabolic disease, seriously posing healthy burdens to the public, whereas interventions available for it are limited to date. Patchouli oil had been reported to attenuate hepatic steatosis in our previous study. beta-patchoulene (beta-PAE) is a representative component separated from patchouli oil with multiple activities, but its effect against NAFLD is still unknown. To investigate the effect and potential mechanism of beta-PAE on NAFLD, we used high fat diet (HFD) in vivo and free fatty acid (FFA) in vitro to induce hepatic steatosis in rats and L02 cells, respectively. Histological examination was evaluated via Hematoxylin-eosin and oil red O staining. The parameters for hepatic steatosis were estimated via biochemical kits, western blotting and quantitative real-time PCR. Compound C, the inhibitor of AMPK, was applied further to examine the precise mechanism of beta-PAE on NAFLD. Our results indicated that beta-PAE significantly attenuated HFD-induced weight gain, hepatic injury, lipid deposition in serum and hepatic tissue as well as FFA induced-lipid accumulation. Besides, beta-PAE markedly improved the expression of AMP-activated protein kinase (AMPK) and its downstream factors which correlate with hepatic lipid synthesis and oxidation in vivo and in vitro. Nevertheless, Compound C abrogated the benefits derived from beta-PAE in L02 cells. In conclusion, these results suggest that beta-PAE exerts AMPK agonist-like effect to regulate hepatic lipid synthesis and oxidation, eventually prevent NAFLD progression.

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