Network pharmacology and experimental verification-based strategy to explore the underlying mechanism of Liu Jun An Wei formula in the treatment of gastrointestinal reactions caused by chemotherapy for colorectal cancer

Li, Gaobiao; Liu, Liying; Yin, Yong; Wang, Mengmeng; Wang, Lei; Dou, Jun; Wu, Hongwei; Yang, Yufei; He, Bin

doi:10.3389/fphar.2022.999115

Cited by 3 publications

(1 citation statement)

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“…Thereby, novel drugs developed with specific ingredients greatly improve clinical efficacy and reduce toxicity and side effect. For example, the underlying mechanism of Liu Jun An Wei formula in treating gastrointestinal reactions caused by chemotherapy for colorectal cancer is explored by network pharmacology ( 38 ). Besides, He et al revealed that Danshen promoted JAL-STAT signaling pathway to treat anemia according to network pharmacology ( 39 ).…”

Section: Discussionmentioning

confidence: 99%

Hedysarum multijugum Maxim treats ulcerative colitis through the PI3K-AKT and TNF signaling pathway according to network pharmacology and molecular docking

Zhang¹,

Chong²,

Xie³

et al. 2022

Ann Transl Med

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Background: Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) that prevails mainly in western countries. Due to the unknown etiology of UC, the purpose of treatments has predominantly comprised symptomatic and pain relief. With extensive research focusing on the pathogenesis of UC, various novel treatments have emerged, although their efficiency has remained unsatisfactory. Hedysarum multijugum Maxim (HMM), a crucial constituent of traditional Chinese medicine, has a broad application in many diseases and has been found beneficial for UC patients.Methods: In this study, network pharmacology and molecular docking analyses were applied to explore the potential mechanism of HMM treating UC. Active ingredients of HMM and target genes were acquired from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP).UC-related genes were obtained from three disease databases. Common genes were selected from these two gene sets, and a compound-genes network was drawn by Cytoscape. Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO) enrichment, and protein-protein interaction (PPI) analyses were performed to identify the essential pathways and proteins in UC.Results: A total of 121 genes were found related to UC and targeted by HMM. The GO and KEGG analyses showed that these genes were associated with inflammation and immune signaling pathways and inflammation-related biological processes (BP) such as the tumor necrosis factor (TNF) and PI3K-AKT signaling pathways. Four active ingredients (quercetin, kaempferol, formononetin, and isorhamnetin) and five genes (RELA, MAPK14, MAPK1, JUN, AKT1) were reserved after screening. Molecular docking further showed that the receptor had a high binding affinity with HMM active ingredients.Conclusions: This study revealed that HMM treats UC through four active ingredients (quercetin, kaempferol, formononetin, and isorhamnetin) targeting five hub genes (RELA, MAPK14, MAPK1, JUN, AKT1) by regulating the PI3K-AKT1 and TNF signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Hedysarum multijugum Maxim treats ulcerative colitis through the PI3K-AKT and TNF signaling pathway according to network pharmacology and molecular docking

Zhang¹,

Chong²,

Xie³

et al. 2022

Ann Transl Med

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Combining network pharmacology and experimental verification to study the anti‐colon cancer effect and mechanism of sulforaphene

Qu,

Li,

et al. 2024

J Sci Food Agric

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BACKGROUNDSulforaphene is a derivative of glucosinolate and a potential bioactive substance used for treating colon cancer. This study aimed to evaluate the potential inhibitory effect and mechanisms of sulforaphene in human colon cancer Caco‐2 cells. Network pharmacology, molecular docking, and experimental verification were performed to elucidate potential sulforaphene mechanisms in the treatment of this condition.RESULTNetwork pharmacology predicted 27 intersection target genes between sulforaphene and colon cancer cell inhibition. Key sulforaphene targets associated with colon cancer cell inhibition were identified as EGFR, MAPK14, MCL1, GSK3B, PARP1, PTPRC, NOS2, CTSS, TLR9, and CTSK. Gene ontology functional enrichment analysis revealed that the above genes were primarily related to the positive regulation of peptidase activity, cytokine production in the inflammatory response, and the cell receptor signaling pathway. Kyoto Encyclopedia of Genes and Genomes enrichment analysis indicated that sulforaphene mainly inhibited the proliferation of cancer cells by affecting apoptosis as well as the signaling pathways of PD‐1, Toll‐like receptor, T cell receptor, and P13k–Akt. Molecular docking results further confirmed that CTSS, GSK3B, and NOS2 were significantly up‐regulated and had good binding affinity with sulforaphene. In vitro experiments also indicated that sulforaphene had a significant inhibitory effect on human colon cancer Caco‐2 cells.CONCLUSIONThis paper revealed the pharmacodynamic mechanism of sulforaphene in the treatment of colon cancer for the first time. It provides scientific insight into the development of sulforaphene as a medicinal resource. © 2024 Society of Chemical Industry.

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Unveiling the therapeutic potential of airpotato yam rhizome against colorectal cancer: a network pharmacology approach

Xie,

Xu,

Chen

et al. 2024

Front. Oncol.

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ObjectiveThe objective of this investigation was to elucidate the key active compounds and molecular mechanisms underlying the therapeutic potential of airpotato yam rhizome (AYR) in colorectal cancer (CRC) treatment.MethodsBy utilizing network pharmacology and molecular docking, key targets and signaling pathways of AYR against CRC were predicted and subsequently validated in cellular and mouse xenograft models.ResultsThis study initially predicted that quercetin was the primary compound in AYR that might have potential efficacy against CRC and that EGFR and AKT1 could be the main targets of AYR, with the EGF/EGFR-induced PI3K/AKT signaling pathway potentially playing a crucial role in the anti-CRC effects of AYR. Molecular docking analysis further indicated a strong binding affinity between quercetin and EGFR, primarily through hydrogen bonds. Additionally, the AYR-derived drug-containing serum was found to inhibit the PI3K/AKT signaling pathway, as demonstrated by decreased levels of p-PI3K, p-AKT, and BCL2, which ultimately led to enhanced apoptosis of HCT116 and HT29 cells. The potential antitumor effects of AYR were investigated in nude mouse xenograft models of human HCT116 and HT29 cells, in which AYR was found to induce tumor cell apoptosis and inhibit tumor formation.ConclusionAYR may promote CRC cell apoptosis by suppressing the PI3K/AKT signaling pathway, which provides a basis for further research on the safe and effective use of AYR for the treatment of CRC.

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Network pharmacology and experimental verification-based strategy to explore the underlying mechanism of Liu Jun An Wei formula in the treatment of gastrointestinal reactions caused by chemotherapy for colorectal cancer

Cited by 3 publications

References 47 publications

Hedysarum multijugum Maxim treats ulcerative colitis through the PI3K-AKT and TNF signaling pathway according to network pharmacology and molecular docking

Hedysarum multijugum Maxim treats ulcerative colitis through the PI3K-AKT and TNF signaling pathway according to network pharmacology and molecular docking

Combining network pharmacology and experimental verification to study the anti‐colon cancer effect and mechanism of sulforaphene

Unveiling the therapeutic potential of airpotato yam rhizome against colorectal cancer: a network pharmacology approach

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