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Exploration of the mechanism of the Mongolian medicine Tonglaga-5 (-5) for the treatment of n-methyl-n'-nitro-n-nitrosoguanidine-induced chronic atrophic gastritis based on network pharmacology and metabolomics.

Cheng Ziqi·Dong Xin·Temuribagen·X U Caimeng·H U Shaonan·Chen Qianwen·Wang Yuewu·Wang Haibo·H E Xiaoyu·Xue Dan·Xue Peifeng
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Abstract

OBJECTIVE: To explore the mechanism of Tonglaga-5 (-5, TLG-5) for the treatment of chronic atrophic gastritis (CAG), based on network pharmacology and metabolomics. METHODS: Forty-eight male Sprague-Dawley rats were randomly divided into six groups (n = 8): control group; model group; teprenone group, and low-, median-, and high- dose TLG-5 groups. The enzyme linked immunosorbent assay (ELISA) was used to measure the expression of pepsinogen &#x2160; (PG &#x2160;), pepsinogen &#x2161; (PG &#x2161;) and gastrin-17 (G-17) in the serum. Hematoxylin and eosin staining were performed to observe the pathological condition. And the network pharmacology was employed to identify the targets and signaling pathways of TLG-5 affecting CAG. Then, the metabolomics approach was applied to explore the specific metabolites and metabolic pathways. Finally, validation was performed using the "metabolite-gene" interaction network, molecular docking and quantitative real-time polymerase chain reaction (qPCR). RESULTS: High-dose TLG-5 significantly improved the expression of PG &#x2160;, PGR (PG &#x2160;/ PG &#x2161;) and G-17 (P < 0.05) and inhibited the expression of phosphoinositide-3-kinase regulatory subunit 2, AKT serine/threonine kinase (AKT), hypoxia-inducible factor 1-alpha (HIF-1&#x3b1;) (P < 0.05). Further, high-dose TLG-5 reduced the number of glands was reduced, and fibrosis with oedema and ecchymosis appeared at the base. Overlapping TLG-5 and CAG gene targets produced 270 interactive targets. The results of gene ontology and Kyoto encyclopedia of genes and genomes enrichment analyses suggested that TLG-5 could affect CAG through the predominantly cancer and inflammation-related pathways. Pyrimidine metabolism was identified as a significantly differential pathway in the mechanism of TLG-5 for treating CAG. CONCLUSIONS: TLG-5 exerts a therapeutic effect on CAG by regulating &#x3b2;-alanine metabolism, pyrimidine metabolism pathways, and inhibiting the PI3K-AKT signaling pathway and HIF-1 signaling pathways.

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AnimalsRats, Sprague-DawleyMaleRatsGastritis, AtrophicDrugs, Chinese HerbalMetabolomicsNetwork PharmacologyHumansGastrinsSignal TransductionHypoxia-Inducible Factor 1, alpha SubunitPepsinogen AMedicine, Mongolian TraditionalChronic DiseaseProto-Oncogene Proteins c-aktTonglaga-5gastritis, atrophicmetabolomicsnetwork pharm-acologyreal-time polymerase chain reactionJournal Article

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Cheng Ziqi, Dong Xin, Temuribagen, X U Caimeng, H U Shaonan, Chen Qianwen, Wang Yuewu, Wang Haibo, H E Xiaoyu, Xue Dan, Xue Peifeng. 2025. Exploration of the mechanism of the Mongolian medicine Tonglaga-5 (-5) for the treatment of n-methyl-n'-nitro-n-nitrosoguanidine-induced chronic atrophic gastritis based on network pharmacology and metabolomics.. https://doi.org/10.19852/j.cnki.jtcm.20250508.001

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