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Author(s): Yogesh Kumar

Email(s): yogeshkumarsahu1222@gmail.com

Address:

    School of Pharmacy, Rungta College of Pharmaceutical Sciences and Research, Rungta International Skills University, Kohka, Bhilai, - 490024, India

Published In:   Volume - 3,      Issue - 2,     Year - 2026

DOI: Not Available

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ABSTRACT:
Ulcerative colitis (UC) is character raised by changes in the immune system and the complete destruction of the intestinal mucosa. A long-term impact is inevitable. Terminalia chebulagic bioactive ellagitannin chebulagic acid (CA) may have anti-inflammatory or anti-free radical properties. Drugs for CA target and UC preventative measures were identified using network pharmacology. We have performed an analysis using Gene Ontology (GO), KEGG pathway enrichment, and proteins-protein link networks. Examining health and illness databases was the first step in the hunt for UC genes. The CA-UC contacts network contains a number of nodes associated with TNF, IL6, IL1B, PTGS2, NFKB1, and AKT1. Through its effects on the NF-κB, TNF, IL-17, MAPK, and PI3K-Akt receptors, enrichment testing demonstrates that CA influences inflammatory responses, cytokine signal ling, oxidative stress, and epithelial protection. New molecular docking experiments show that California interacts strongly with key inflammatory proteins. Among CA's several beneficial effects in UC include alterations to the immune system, an increase in natural inflammation, and the restoration of mucosal integrity. The molecular process provides an explanation for a treatment benefit. An inflammation-relieving polyphenol found in Terminalia, CA may help those suffering from ulcerative colitis. No one has a clue as to how it functions. Network pharmacology specialists looked at how CA affected UC. Predicted therapeutic targets were identical, according to protein-protein interaction networks, CA-UC gene matching, and enrichment analysis. A number of proteins are located within the CA-UC network. These include NFKB1, PTGS2, IL1B, IL6, and TNF. Research from the GO and KEGG databases indicates that CA has the potential to influence pathways like NF-κB, TNF, MAPK, and PI3K-Akt. Repair of the epithelium, responses to oxidative stress, immunological control, and inflammatory signal ling are all impacted by these pathways. Further research is necessary to confirm the therapeutic potential of CA for UC however it has the ability to decrease inflammation and mucosal dynamics.

Cite this article:
Kumar, Y. A Network Pharmacology-Based Investigation into the Mechanism of Chebulagic Acid in the Treatment of Ulcerative Colitis. Probecell Sci.,2026;3(2):1–14.


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