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Rosmarinic acid attenuates hyperuricemia-induced intestinal damage by activating mitophagy via the p38 MAPK/mTOR
Jian Guo1, Meihan Zhang1, Yuanhang Cheng1
1State Key Laboratory of Marine Food Processing and Safety Control, National Engineering Research Center of Seafood, School of Food Science and Technology, Dalian Polytechnic University, Dalian, Liaoning 116034, China.
Abstract:
Intestinal damage is commonly associated with hyperuricemia (HUA). This study investigated the effect of rosmarinic acid (RA) on intestinal damage in a high-purine diet (HPD)-induced HUA mouse model and the underlying mechanisms. RA effectively alleviated HUA and its related intestinal mucosal damage, epithelial cell apoptosis, and mitochondrial dysfunction in mice. RA also restored the membrane localization of ATP-binding cassette subfamily G member 2 (ABCG2) in epithelial cells. Mechanistically, RA inhibited intestinal epithelial cell apoptosis by modulating the p38 MAPK/mTOR signaling pathway and activating mitophagy. Cellular thermal shift assay (CETSA) and drug affinity responsive target stability (DARTS) assay supported the direct interaction between RA and dual specificity phosphatase 1 (DUSP1), while functional validation further reinforced the involvement of DUSP1 in RA-mediated regulation of the p38 MAPK/mTOR pathway. These findings suggest that RA could be developed as a therapeutic option for HUA and its associated intestinal damage.
