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Ginsenoside R3 alleviates non-alcoholic fatty liver disease by regulating the PPARγ/miR-103-3p pathway


Chenyi Li
Danjun Fan

Abstract

Purpose: To determine the effect of ginsenoside R3 (Rg3) on non-alcoholic fatty liver disease (NAFLD), and the mechanism involved.


Methods: High-fat diet (HFD) was used to establish an NAFLD mouse model. The mice were daily and intraperitoneally injected with Rg3  at a dose of 1 mg/kg. Blood lipid levels and levels of liver inflammatory markers were measured by enzyme-linked immunosorbent assay  (ELISA) while liver pathological changes and lipid accumulation were assessed with hematoxylin-eosin (H&E) staining and oil red O  staining, respectively. The mRNA and protein expressions of miR-103-3p and PPARγ were determined with quantitative real-time  polymerase chain reaction (qPCR) and western blot assay, respectively. Furthermore, an in vitro hepatocyte NAFLD model was  established, and Rg3 was used to treat the cells; PPARγ was overexpressed in the cells. Lipid accumulation, inflammatory factors, as well as PPARγ and miR-103-3p expressions were assessed as indicated for the in vivo studies above. Apoptosis was determined by flow  cytometry.


Results: Rg3 alleviated the NAFLD-induced decreases in liver function, reversed NAFLD-mediated pathological injury in liver  tissue injury, and decreased hepatic lipid build-up and inflammatory lesions (p < 0.05). It also significantly reversed the upregulation of  PPARγ and miR-103-3p in the liver tissue of NAFLD mice. At the cellular level, Rg3 significantly inhibited free fatty acid (FFA)-induced lipid accumulation, apoptosis and inflammatory factors in primary mouse hepatocytes. The PPARγ overexpression counteracted the inhibitory  effect of Rg3 on hepatocyte apoptosis, and increased miR103-3p expression (p < 0.05).


Conclusion: These data suggest that Rg3 mitigates  NAFLD through regulation of the PPARγ/miR-103- 3p pathway. Therefore, Rg3 may be suitable for the treatment of NAFLD.  However, clinical trials are required to ascertain the validity of this therapeutic strategy in clinical practice.   


Journal Identifiers


eISSN: 1596-9827
print ISSN: 1596-5996