Treatment of Acute Ulcerative Colitis with Zinc Hyaluronate in Mice
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Ulcerative colitis (UC) is a type of inflammatory bowel disease arising from numerous factors, while UC patients face insufficient treatment options and a high incidence of adverse reactions to the current therapies. As a functional food additive, hyaluronic acid plays a certain role in intestinal repair. In this study, we constructed a mouse model of dextran sulfate sodium (DSS)-induced UC to examine the effects and underlying mechanisms of action of zinc hyaluronate (ZnHA) on the pathogenesis of UC. ZnHA effectively alleviated key clinical UC symptoms, such as weight loss, loose stools, and bloody stools. Mechanistically, ZnHA attenuated the expression of inflammatory factors, such as tumor necrosis factor-α, interleukin (IL)-6, and myeloperoxidase while upregulating the expression of IL-10. Furthermore, through intestinal flora and short-chain fatty acid analyses, ZnHA was found to promote propionic acid production by enriching beneficial bacteria. ZnHA simultaneously enhanced the expression of tight junction proteins, specifically ZO-1 and occludin, thereby restoring intestinal barrier function. Overall, our findings elucidate the therapeutic potential of ZnHA in treating acute UC by inhibiting intestinal inflammation and regulating flora, while also providing further theoretical support for development of hyaluronic acid to treat this disease.
Abstract
Ulcerative colitis (UC) is a type of inflammatory bowel disease arising from numerous factors, while UC patients face insufficient treatment options and a high incidence of adverse reactions to the current therapies. As a functional food additive, hyaluronic acid plays a certain role in intestinal repair. In this study, we constructed a mouse model of dextran sulfate sodium (DSS)-induced UC to examine the effects and underlying mechanisms of action of zinc hyaluronate (ZnHA) on the pathogenesis of UC. ZnHA effectively alleviated key clinical UC symptoms, such as weight loss, loose stools, and bloody stools. Mechanistically, ZnHA attenuated the expression of inflammatory factors, such as tumor necrosis factor-α, interleukin (IL)-6, and myeloperoxidase while upregulating the expression of IL-10. Furthermore, through intestinal flora and short-chain fatty acid analyses, ZnHA was found to promote propionic acid production by enriching beneficial bacteria. ZnHA simultaneously enhanced the expression of tight junction proteins, specifically ZO-1 and occludin, thereby restoring intestinal barrier function. Overall, our findings elucidate the therapeutic potential of ZnHA in treating acute UC by inhibiting intestinal inflammation and regulating flora, while also providing further theoretical support for development of hyaluronic acid to treat this disease.