Self-crosslinking hyaluronic acid hydrogel as an enteroprotective agent for the treatment of inflammatory bowel disease

The pathological changes in inflammatory bowel disease (IBD) include the disruption of intestinal barrier function and the infiltration of pathogenic microbes. The application of an artificial protective barrier at the site of inflammation can prevent bacterial infiltration, promote epithelial cell...

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Veröffentlicht in:International journal of biological macromolecules 2024-07, Vol.273 (Pt 2), p.132909, Article 132909
Hauptverfasser: Zhang, Guangshuai, Song, Dandan, Ma, Ruilong, Li, Mo, Liu, Bingyang, He, Zhonggui, Fu, Qiang
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Sprache:eng
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Zusammenfassung:The pathological changes in inflammatory bowel disease (IBD) include the disruption of intestinal barrier function and the infiltration of pathogenic microbes. The application of an artificial protective barrier at the site of inflammation can prevent bacterial infiltration, promote epithelial cell migration, and accelerate wound healing. In this study, dopamine-modified hyaluronic acid (HA-DA) was developed as a bioadhesive self-cross-linkable hydrogel, which acted as an enteroprotective agent to promote the healing of inflamed intestinal tissue. The adhesion strength HA-DA to mouse colon was 3.81-fold higher than HA. Moreover, HA-DA promoted Caco-2 cell proliferation and migration as well as had a strong physical barrier effect after gelation. After oral administration, the HA-DA reduced weight loss and attenuated impaired goblet cell function in mice with dextran sodium sulfate-induced IBD. In addition, HA-DA promoted restoration of the epithelial barrier by the upregulation of tight junction proteins. The results reported herein substantiated that self-cross-linkable hydrogel-based enteroprotective agents are a promising approach for the treatment of IBD. Dopamine-modified hyaluronic acid-based self-cross-linkable hydrogel for the treatment of inflammatory bowel disease. After oral administration, the hydrogel would adhere to the intestinal surface, prevent the invasion of pathogenic bacteria, and promote epithelial barrier recovery. [Display omitted]
ISSN:0141-8130
1879-0003
1879-0003
DOI:10.1016/j.ijbiomac.2024.132909