, thereby enhancing the production of acetate, propionate, and butyrate. Molecular analyses demonstrated that Dn downregulated the expression of URAT1 while upregulating ABCG2, thereby promoting UA excretion. Histopathological evaluation confirmed that Dn restored the glomerular atrophy, tubular dilation, and collagen deposition induced by HUA. These findings suggest that Dn is a promising multitarget therapeutic agent for HUA and provides a scientific foundation for the development of novel microbiome-based strategies against HUA.
Cheng et al. (Wed,) studied this question.