Unveiling the molecular mechanisms of Dendrobium officinale polysaccharides on intestinal immunity: An integrated study of network molecular and in vivo experiments

文献类型： 外文期刊

第一作者： Yang, Chenchen

作者： Yang, Chenchen;Li, Jingrui;Luo, Mengfan;Zhou, Wanyi;Xing, Jianrong;Yang, Ying;Tao, Wenyang;Wang, Lu;Rao, Wenjia

作者机构：

关键词： Dendrobium officinale polysaccharides; Intestinal immunity; Network pharmacology; Molecular docking and simulation; Mice model

期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：7.7； 五年影响因子：7.7 ）

ISSN： 0141-8130

年卷期： 2024 年 276 卷

页码：

收录情况： SCI

摘要： Intestinal immunity plays a pivotal role in overall immunological defenses, constructing mechanisms against pathogens while maintaining balance with commensal microbial communities. Existing therapeutic interventions may lead to drug resistance and potential toxicity when immune capacity is compromised. Dendrobium officinale, a traditional Chinese medicine, contains components identified to bolster immunity. Employing network pharmacology strategies, this study identified constituents of Dendrobium officinale and their action targets in the TCMSP and Swiss Target Prediction databases, and compared them with intestinal immunity-related targets. Protein-protein interaction networks revealed the core targets of Dendrobium officinale polysaccharides, encompassing key pathways such as cell proliferation, inflammatory response, and immune reactions, particularly in association with the Toll-like receptor 4. Molecular docking and molecular dynamics simulation further confirmed the high affinity and stability between Dendrobium officinale polysaccharides and Toll-like receptor 4. In vivo experiments demonstrated that Dendrobium officinale polysaccharides modulates the expression of Tolllike receptor 4 and its downstream key proteins in the colonic mucosa of mice. Consequently, these findings suggest that Dendrobium officinale polysaccharides may serve as a potential modulator for intestinal immune functions, with its mechanism potentially related to the Toll-like receptor 4.

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