Journal of Practical Hepatology ›› 2024, Vol. 27 ›› Issue (6): 816-819.doi: 10.3969/j.issn.1672-5069.2024.06.005

• Hepatitis in animal • Previous Articles     Next Articles

Down-regulation of hepatic SREBP1 and PPAR-γ expression by naringin in mice with high-fat diet-induced NAFLD

Jia Jihui, Zhang Yizhi, Lin Jing, et al   

  1. Fourth Department of Liver Disease, You’an Hospital, Capital Medical University, Beijing 100069, China
  • Received:2024-03-18 Online:2024-11-10 Published:2024-11-07

Abstract: Objective The purpose of this experiment was to investigate effects of naringin (Nar) on lipid metabolism in mice with high-fat diet (HFD) induced non-alcoholic fatty liver diseases (NAFLD). Methods Twenty-four C57BL/6J mice were randomly divided into control, model and HFD/Nar-intervention groups, with eight mice in each group. The model of NAFLD was established by HFD intake, and the intervention was carried out by naringin gavage at dose of 100 mg.kg-1 for four weeks. Drug intervention with differential gene enrichment pathways was determined by transcriptome sequencing. Hepatic lipid metabolism related genes and their protein expression were detected by qPCR and Western blot. Results Body mass of mice in model group increased by 57.8% (P<0.01) as compared with in the control, while in naringin-intervention group, it decreased by 13.5% (P<0.01); hepatic TG and TC levels in the model were (3.5±0.4)mmol/g protein and (3.1±0.5)mmol/g protein, both much higher than [(1.0±0.3)mmol/g protein and (0.8±0.1)mmol/g protein, P<0.01] in the control, while in HFD/Nar-intervention group, they significantly decreased to [(2.1±0.4)mmol/g protein and (1.11±0.3)mmol/g protein, P<0.05]; KEGG enrichment analysis by transcriptome sequencing showed obvious impacts of naringin on nine pathways related to lipid metabolism, presenting with hepatic sterol regulatory element binding protein 1 (SREBP1), peroxisome proliferator-activated receptor-γ (PPAR-γ), thrombospondin receptor (CD36) and liver-type fatty acid-binding protein 1 (FABP1) down-regulation(P<0.05), and PPAR-α and recombinant carnitine palmitoyltransferase 1A (CPT-1A) up-regulation(P<0.05). Conclusion Naringin could significantly ameliorate hepatic lipid deposition, the mechanisms by which it work might be related to regulation of some gene expression and inhibit lipid uptake and synthesis, and accelerate fatty acid oxidation.

Key words: Non-alcoholic fatty liver diseases, Naringin, Sterol regulatory element binding protein 1, Peroxisome proliferator-activated receptor-γ, Liver-type fatty acid-binding protein 1, Recombinant carnitine palmitoyltransferase 1A, Mice