Jun Qi1, 2,
Jiali Liu2,
Feng Bai1,
Xiaowen Song2,
Shufang Niu2,
Jianfang Sun1,
Wanfu Bai1, 2, 3
For correspondence:- Wanfu Bai Email: 102010114@btmc.edu.cn
Received: 20 June 2025 Accepted: 11 October 2025 Published: 31 October 2025
Citation: Qi J, Liu J, Bai F, Song X, Niu S, Sun J, et al. In silico assessment of cinnamon compounds in ulcerative colitis therapy. Trop J Pharm Res 2025; 24(10):1261-1269 doi: https://dx.doi.org/10.4314/tjpr.v24i10.6
© 2025 The authors.
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Purpose: To identify potential quality markers (Q-markers) of cinnamon for treating ulcerative colitis (UC) using network pharmacology methodologies and evaluate potential therapeutic markers. Methods: The GeneCards, Online Mendelian Inheritance in Man (OMIM), and Therapeutic Target Databases (TTD) were employed to identify potential targets and pathways associated with the active components of cinnamon. A multi-component-target interaction network was developed using Cytoscape, and core compounds were evaluated through topological analysis. Molecular docking and visualization analyses of core compounds and key targets were conducted using AutoDock Tools and PyMol to identify potentially therapeutically active components. Results: A total of 18 active components of cinnamon and 74 UC-related targets were identified. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that the mechanisms predominantly involve the PI3K-Akt, HIF-1, and JAK-STAT signaling pathways. Molecular docking demonstrated that cinnamates, ellagic acid, and epigallocatechin gallate significantly bind to core targets (e.g., AKT1, STAT3), indicating their potential as Q-markers in treating UC. Conclusion: This study comprehensively clarifies the mechanisms through which cinnamon acts on UC, involving the PI3K-Akt, HIF-1, and JAK-STAT signaling pathways. These mechanisms provide a scientific foundation for optimizing the quality standards of cinnamon and its formulations.