Abstract
Background Gastric carcinoma (GC) is a kind of digestive tract tumor that is highly malignant and has a very poor prognosis. Although both Astragalus mongholicus (AM, huáng qí) and Curcuma phaeocaulis Valeton (CPV, é zhú) 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.
Highlights
Gastric carcinoma (GC) is one of the five most common cancers in the world
If the compounds did not meet the screening criteria or does not exist in the TCM system pharmacology database and analysis platform (TCMSP) database, it would be supplemented from the TCMID and the active components of AM-CPV drug-pair reported in the related literature were included in [11, 12]. e related compounds were input into PubChem and PharmGKB Database to obtain the molecular structure of the compounds
Targets Prediction and Analysis of AM and CPV. 428 core active components of AM and 24 CPV (Supplementary Table 2) were obtained from TCMSP. 24 AM and 9 CPV ingredients were obtained from TCMID. 2 CPV ingredients were obtained from relating literature. rough SwissTargetPrediction and STITCH database, 166 active components of AM and 81 active components of CPV (Supplementary Table 3) were obtained. 30 active components of AM and 38 active components of CPV (Supplementary Table 4) were obtained from ETCM
Summary
Gastric carcinoma (GC) is one of the five most common cancers in the world. At present, about 1.03 million patients suffer from GC [1]. Gastric carcinoma (GC) is a kind of digestive tract tumor that is highly malignant and has a very poor prognosis Both Astragalus mongholicus (AM, huang qı) and Curcuma phaeocaulis Valeton (CPV, ́e zhu) can slow the onset and progression of GC, the mechanism by which AM-CPV works in the treatment of GC is uncertain. 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. 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
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