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

Abstract

Abstract The main aim of this study was to explore the antitumor effects and mechanism of 1,2,3,4,6-Penta-O-galloyl-β-D-glucose on human hepatocellular carcinoma HepG2 cells. A network pharmacology method was first used to predict the possible inhibition of hepatocellular carcinoma growth by β-PGG through the p53 signaling pathway. Next, the 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, and intracellular Ca2+ concentration; and real-time fluorescence quantification and immunoblotting were performed to evaluate changes in the expression of P53, BAX, and BCL-2. Results showed that the expression of P53 genes and proteins associated with the p53 signaling pathway was significantly increased by β-PGG treatment. It was found that β-PGG significantly inhibited survival of HepG2 cells, promoted apoptosis, decreased mitochondrial membrane potential and intracellular Ca2+ concentration, upregulated P53 gene and protein expression, increased CASP3 expression, and induced apoptosis in HepG2 cells. In conclusion, this study has shown that network pharmacology can accurately predict the target of β-PGG's anti-hepatocellular carcinoma action. Moreover, it was evident that β-PGG can induce apoptosis in HepG2 cells by activating the p53 signaling pathway to achieve its anti-hepatocellular carcinoma effect in vitro.