Mechanism of Herb Pairs and Valeton in Treating Gastric Carcinoma: A Network Pharmacology Combines with Differential Analysis and Molecular Docking.

BACKGROUND

Gastric carcinoma (GC) is a kind of digestive tract tumor that is highly malignant and has a very poor prognosis. Although both (AM, ) and Valeton (CPV, ) can slow the onset and progression of GC, the mechanism by which AM-CPV works in the treatment of GC is uncertain.

MATERIALS AND METHODS

The traditional Chinese medicine network databases TCMSP, TCMID, and ETCM were used to identify the key functional components and associated targets of AM and CPV. To establish a theoretical foundation, the development of gastric cancer (GC) was predicted utilizing a GEO gene chip and TCGA difference analysis mixed with network pharmacology. A herbal-ingredient-target network and a core target-signal pathway network were created using GO and KEGG enrichment analyses. The molecular docking method was used to evaluate seventeen main targets and their compounds.

RESULTS

Cell activity, reactive oxygen species modification, metabolic regulation, and systemic immune activation may all be involved in the action mechanism of the AM-CPV drug-pair in the treatment of GC. It inhibits the calcium signaling route, the AGE-RAGE signaling system, the cAMP signaling pathway, the PI3K-Akt signaling network, and the MAPK signaling pathway, slowing the progression of GC. The number of inflammatory substances in the tumor microenvironment is reduced, GC cell proliferation is deprived, apoptosis is promoted, and GC progression is retarded through controlling the IL-17 signaling route, TNF signaling pathway, and other inflammation-related pathways.

CONCLUSIONS

The AM-CPV pharmaceutical combination regulates GC treatment via a multitarget, component, and signal pathway with a cooperative and bidirectional regulatory mechanism. Its active constituents may treat GC by regulating the expression of STAT1, MMP9, IL6, HSP90AA1, JUN, CCL2, IFNG, CXCL8, and other targets, as well as activating or inhibiting immune-inflammatory and cancer signaling pathways.