Exploration of the effect and mechanism of psoralidin against nasopharyngeal carcinoma based on network pharmacology, molecular docking and in vitro experiments

Objective:To explore the effect and molecular mechanism of psoralidin(PSO)in the treatment of na-sopharyngeal carcinoma based on network pharmacology and bioinformatics.Methods:The nasopharyngeal car-cinoma 5-8F cells were divided into 5-8F group (0 μmol/L PSO), low-dose PSO group (10 μmol/L group), mid-dle-dose PSO group (20 μmol/L group) and high-dose PSO group (30 μmol/L group).The effect of PSO on the proliferation and clone formation of nasopharyngeal carcinoma 5-8F cells was explored by CCK-8 and plate clon-ing.Pubchem, Pharmmapper and GeneCards databases got the potential target of PSO in the treatment of naso-pharyngeal carcinoma; DAVID database carried out GO and KEGG analysis; STRING, GEPIA databases and Cy-toscape software constructed a network diagram and got the core target; molecular docking and western blotting were used to verify the core targets and main pathways.Results:PSO inhibited the proliferation of 5-8F cells in a concentration-dependent manner.Compared with 5-8F group, the ability of cell clone formation in each dose group of PSO decreased(P< 0.05).There were 66 potential targets of PSO in the treatment of nasopha-ryngeal carcinoma, and KEGG analysis shows that it was closely related to PI3K-Akt signal pathway.The core targets were ALB, HSP90AA1, SRC, EGFR, CASP3, ANXA5 and MAPK1, among which ALB, HSP90AA1 and ANXA5 were survival-related targets; PSO had good binding ability with the core targets ALB, HSP90AA1 and ANXA5.Compared with the 5-8F group, the expressions of PI3K, p-PI3K, Akt and p-Akt protein in the highdose PSO group decreased(P< 0.05).Conclusion:PSO can effectively inhibit the proliferation and clone forma-tion of nasopharyngeal carcinoma 5-8F cells, and its anti-nasopharyngeal carcinoma mechanism is mainly related to the inhibition of PI3K-Akt signal pathway activity.