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CN 22-1108/R
Volume 41 Issue 3
Mar.  2025
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Article Navigation >  Journal of Clinical Hepatology  > 2025  >  41(3): 499-505

Study on the protective efect and mechanism of paeoniflorin on palmitic acid-induced HepG2 cells

DOI: 10.12449/JCH250316
  • 1.

    Department of Hepatobiliary，Spleen and Stomach Diseases，The First Affiliated Hospital of Henan University of Chinese Medicine，Zhengzhou 450003，China

  • 2.

    The First Clinical Medical College of Henan University of Chinese Medicine，Zhengzhou 450046，China

Research funding:

National Natural Science Foundation of China (82205086);

Key Project of Traditional Chinese Medicine Science Research in Henan Province (2022JDZX006);

Project of Henan Provincial Health Commission (2022JDZX114);

Henan Province Science and Technology Attack Fund (232102310438)

More Information
  • Corresponding author: ZHAO Wenxia， zhao-wenxia@163.com （ORCID： 0000-0001-6666-9469）
  • Received Date: 2024-07-08
  • Accepted Date: 2024-07-29
  • Published Date: 2025-03-25
    Abstract
  •   Objective  To investigate the role and mechanism of action of paeoniflorin （PF） in protecting HepG2 cells induced by palmitic acid （PA）.  Methods  HepG2 cells were stimulated with PA at a concentration of 250 μmol/L to establish a NAFLD model. Compound C at a concentration of 10 μmol/L was used as an inhibitor， and PF at a concentration of 25 μmol/L was used for intervention. The experiment was divided into normal group （CON group） treated with complete culture medium， model group （MOD group） treated with PA， PF treatment group （MOD+PF group） treated with PA and PF， model+inhibitor group （MOD+COM group） treated with PA and Compound C， and model+inhibitor+PF group （MOD+COM+PF group） treated with PA， Compound C， and PF. Kits were used to measure lipid deposition indicators， liver function parameters， oxidative stress indicators， and inflammation indicators； oil red O staining was used to observe lipid deposition； Western Blot was used to measure the protein expression levels of AMPK， SIRT1， PGC-1α， mTOR， Beclin-1， LC3， and P62 in cells. The one-way analysis of variance was used for comparison of quantitative data between groups， while the Tukey’s test was used for comparison between two groups.  Results  Compared with the MOD group， PF improved the levels of TC and TG （P<0.05）， reduced the levels of ALT， AST， CRP， TNF-α， IL-1β， and IL-6 （P<0.05）， increased the activity of SOD and CAT and the level of GSH， and reduced the level of MDA in cells （all P<0.05）. Oil red O staining showed that PF alleviated lipid deposition in cells. Western blot results showed that compared with the MOD group， PF increased the protein expression levels of p-AMPK， SIRT1， PGC-1α， LC3Ⅱ/LC3Ⅰ， and Beclin-1 and reduced the protein expression levels of p-mTOR and P62 （all P<0.05）.  Conclusion  PF can inhibit PA-induced oxidative stress and inflammatory response in HepG2 cells， improve lipid deposition， and promote autophagy via the AMPK/SIRT1/PGC-1α/mTOR signaling pathway.

     

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