Anti‐Inflammatory Action and Molecular Mechanism of Fucoidan Against Cystitis Glandularis

Abstract

Cystitis glandularis (CG), known as a pre‐gradual lesion in the bladder, is the pathological changes in the vesical mucosa characterized by inflammatory invasion and chronic obstruction. Clinically, effective treatment against CG is prescribed only when using drug therapy. Fucoidan, the naturally extractive polysaccharide, is well‐reported bioactive compound with anti‐inflammatory and immunoregulatory properties. In this research, an emerging computational approach was applied to explicate anti‐CG actions and pharmacological targets exhibited by fucoidan in detail. Current network pharmacology data showed that 16 intersection genes of fucoidan and CG were identified, whereas all 6 core targets, including interleukin‐6 (IL‐6), tumor necrosis factor (TNF), interleukin‐1B (IL‐1B), matrix metalloproteinase‐9 (MMP‐9), interleukin‐10 (IL‐10), matrix metalloproteinase‐2 (MMP‐2), biological processes, and signaling pathways of fucoidan against CG were characterized, respectively. As revealed in the underlying mechanism, the anti‐CG actions achieved by fucoidan were chiefly implicated in the reduction of inflammatory reactions and enhancement of immunoregulation. Taken together, these network bioinformatics findings may be used to reveal anti‐CG effects and the pharmacological mechanism of fucoidan before further experimental validation. Furthermore, those core genes identified may be therapeutic targets for research and development of fucoidan‐anti‐CG.