In vitro anti-hepatocellular carcinogenesis of 1,2,3,4,6-Penta- O-galloyl-0-D-glucose

Background: 1,2,3,4,6-Penta-O-galloyl-0-D-glucose (0-PGG) is a polyphenol ellagic compound with a vari-ety of pharmacological effects and has an inhibitory effect on lots of cancers.Objective: To explore the antitumor effects and mechanism of 1,2,3,4,6-Penta-O-galloyl-0-D-glucose on human hepatocellular carcinoma HepG2 cells.Design: A network pharmacology method was first used to predict the possible inhibition of hepatocellular carcinoma growth by 1,2,3,4,6-Penta-O-galloyl-0-D-glucose (0-PGG) through the p53 signaling pathway. Next, the Cell Counting Kit (CCK-8) assay was performed to evaluate changes in the survival rate of human hepatocellular carcinoma HepG2 cells treated with different concentrations of the drug; flow cytometry was used to detect changes in cell cycle, apoptosis, mitochondrial membrane potential (MMP) and intracellular Ca2+ concentration; real-time fluorescence quantification and immunoblotting showed that the expression of P53 genes and proteins associated with the p53 signaling pathway was significantly increased by 0-PGG treatment.Reasult: It was found that 0-PGG significantly inhibited survival of HepG2 cells, promoted apopto-sis, decreased MMP and intracellular Ca2+ concentration, upregulated P53 gene and protein expression, increased CASP3 expression, and induced apoptosis in HepG2 cells. Conclusion: This study has shown that network pharmacology can accurately predict the target of 0-PGG's anti-hepatocellular carcinoma action. Moreover, it was evident that 0-PGG can induce apopto-sis in HepG2 cells by activating the p53 signaling pathway to achieve its anti-hepatocellular carcinoma effect in vitro.

Automated summary

By using network pharmacology, this study predicted that 1,2,3,4,6-Penta-O-galloyl-0-D-glucose (0-PGG) may inhibit the growth of hepatocellular carcinoma (HepG2) cells through the p53 signaling pathway. The experimental results confirmed that 0-PGG significantly inhibited the survival of HepG2 cells, promoted apoptosis, and induced apoptosis by activating the p53 signaling pathway.