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Volume 41 Issue 3
Mar.  2025
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Article Navigation >  Journal of Clinical Hepatology  > 2025  >  41(3): 493-498

Effect and mechanism of gallic acid on the proliferation， migration， invasion， and apoptosis of human hepatocellular carcinoma HepG2 cells

DOI: 10.12449/JCH250315

  • Central Laboratory，Hepatobiliary Hospital of Jilin，Changchun 130062，China

Research funding:

Health Science and Health Technology Innovation Project of Jilin Province (2020J082)

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  • Corresponding author: ZHAO Wenjing， xingyuewj@163.com （ORCID： 0000-0002-0841-9362）
  • Received Date: 2024-07-09
  • Accepted Date: 2024-09-19
  • Published Date: 2025-03-25
    Abstract
  •   Objective  To investigate the effect of gallic acid （GA） on the proliferation， migration， invasion， and apoptosis of human hepatocellular carcinoma HepG2 cells and its mechanism.  Methods  HepG2 cells were treated with different concentrations of GA （0， 5， 10， 20， 30， 40， and 50 μg/mL） for 24 and 48 hours， and CCK8 assay was used to measure cell viability and calculate IC50. The experiment was divided into control group （HepG2 cells）， 5 μg/mL GA group， 10 μg/mL GA group， and 20 μg/mL GA group. Plate colony formation assay was used to evaluate the effect of GA on cell proliferation； wound healing assay and Transwell chamber assay were used to observe the effect of GA on cell migration and invasion； flow cytometry was used to observe the effect of GA on cell apoptosis； Western blot was used to measure the expression of matrix metallopeptidase-2 （MMP-2）， matrix metallopeptidase-9 （MMP-9）， and apoptosis-related proteins. A one-way analysis of variance was used for comparison between multiple groups， and the least significant difference t-test was used for further comparison between two groups.  Results  The mean IC50 value of GA on HepG2 cells was 38.02±2.58 μg/mL at 24 hours and 18.36±1.54 μg/mL at 48 hours. The number of cell colonies was 239.00±29.45 in the control group， 210.00±19.00 in the 5 μg/mL GA group， 144.33±16.03 in the 10 μg/mL GA group， and 57.00±9.55 in the 20 μg/mL GA group， suggesting that compared with the control group， each GA group had a significant reduction in cell colony formation ability （all P<0.05）. After 24 hours of treatment， the cell migration rate was 42.62%± 7.82% in the control group， 35.34%±6.42% in the 5 μg/mL GA group， 21.85%±4.42% in the 10 μg/mL GA group， and 12.57%± 3.54% in the 20 μg/mL GA group， respectively， in these four groups， and the number of transmembrane cells in these four groups was 230.30±15.30， 182.12±12.60， 137.20±7.50， and 124.40±6.80， respectively， suggesting that compared with the control group， each GA group had significant reductions in migration rate and the number of transmembrane cells （all P<0.05）. After 48 hours of treatment， the cell apoptotic rate was 0.67%±0.08% in the control group， 13.27%±1.07% in the 5 μg/mL GA group， 20.94%± 2.45% in the 10 μg/mL GA group， and 40.74%±2.63% in the 20 μg/mL GA group， and compared with the control group， each GA group had a significant increase in cell apoptosis rate （all P<0.05）. Compared with the control group， each GA group had significant reductions in the protein expression levels of MMP-2 and MMP-9 （all P<0.05） and significant increases in the protein expression levels of Bax and cleaved caspase-3 （all P<0.05）.  Conclusion  GA can inhibit the proliferation， migration， and invasion of HepG2 cells and promote the apoptosis of HepG2 cells， possibly by regulating MMP-2， MMP-9， and the apoptosis-related proteins Bax/Bcl-2.

     

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