Fortunellin Elevates the AMPK Pathway to Reduce Lipid Deposition and Immune Disorders in Young Non-Alcoholic Fatty Liver Disease Rats.

Introduction: Non-alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease and seriously threatens children's health. Fortunellin exerts a protective role in several human diseases, but its function in NAFLD is unclear. This research tried to uncover Fortunellin's function and mechanism in young NAFLD rats.

Methods: A young rat model of NAFLD was established by administering a high-fat diet (HFD). Also, Fortunellin was delivered via intragastric administration. The effects of Fortunellin on NAFLD were assessed through hematoxylin-eosin staining, analysis of serum levels of ALT, AST, TCH, TG, LDL-C, and HDL-C, Oil Red O staining, Western blot, ELISA, and quantitative real-time PCR (qRT-PCR). Additionally, the Fortunellin mechanism in NAFLD was estimated with Western blot, immunofluorescence, Oil Red O staining, and ELISA assays.

Results: Functionally, Fortunellin (5 or 10 mg/kg) reduced liver injury in young NAFLD rats, which was mainly associated with the gradual decrease of a liver index, the increased liver tissue score, and the gradually decreased serum levels of ALT and AST. Also, Fortunellin restrained NFALD rat dyslipidemia by lessening TCH, TG, LDL-C serum levels, and increasing HDL-C levels. Furthermore, Fortunellin repressed liver lipid metabolism and immune disorders in young NAFLD rats. Mechanically, Fortunellin enhanced the AMPK activation in young NAFLD rats. Additionally, Fortunellin relieved lipid deposition and immune disorders in young NAFLD rats, while compound C (CC, an AMPK inhibitor) abolished these impacts.

Discussion: This study confirmed that Fortunellin alleviated liver injury in young rats with NAFLD, and this might be achieved by activating the AMPK axis. The completion of this study provided a promising drug for the NAFLD treatment.

Conclusion: In summary, Fortunellin alleviated lipid deposition and immune disorders in young rats with NAFLD through the activation of AMPK.