The mechanism of hesperidin against oral squamous cell carcinoma based on network pharmacology
10.3969/j.issn.1001-3733.2024.03.004
- VernacularTitle:基于网络药理学探讨橙皮苷抗口腔鳞状细胞癌作用机制
- Author:
Shuai LIU
1
;
Xiao LI
;
Tao ZHANG
;
Guolin LI
Author Information
1. 154000,佳木斯大学附属口腔医院
- Keywords:
Hesperidin;
Oral squamous carcinoma;
Network pharmacology;
Molecular docking
- From:
Journal of Practical Stomatology
2024;40(3):323-329
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the effects of hesperidin against human tongue squamous cell carcinoma Tca-8113 cells and explore its mechanism of action.Methods:Tca-8113 cells were cultured in vitro with different concentrations of hesperidin.MTT assay and flow cytometry were used to detect the cell proliferation and apoptosis respectively.The potential targets of hesperidin against Tca-8113 cells were studied by network pharmacology.The protein-protein interaction network(PPI)was constructed,gene ontology GO analy-sis,kyoto gene and genome baike encyclopedia(KEGG)enrichment analysis were performed.Q-PCR was used to detect the effect of different concentrations of hesperidin on the related mRNA expression level of Tca-8113 cells.The binding force of hesperidin to the core targets was predicted by molecular docking and a scoring function was used to judge the binding force.Results:Hesperidin inhibi-ted proliferation and promoted apoptosis of Tca-8113 cells(P＜0.05)in a dosedependant manner;KEGG enrichment analysis of the key gene targets involved in the regulation of oral squamous cell carcinoma by hesperidin may be related to PI3K-Akt,MAPK and Ras signaling pathways.Q-PCR results showed that the mRNA expression of MAPK8,HSP90AA1 and MAPK1(ERK2)were significantly different(P＜0.05).Molecular docking results showed that hesperidin had the strongest binding force with MAPK1(ERK2).Conclu-sion:Hesperidin may inhibit the proliferation and promote apoptosis of Tca-8113 cells by regulating Ras/Raf/MEK/ERK signaling pathway.
