Bta-miR-25 alleviates lipopolysaccharide-induced endometritis in cows by targeting DUSP10 to inhibit MAPK signaling.

Bovine endometritis is a common and serious disease that has caused huge economic losses and a decline in production performance in the dairy cattle industry. This study aimed to investigate the regulatory role of bta-miR-25 in Lipopolysaccharide (LPS)-induced BEND and its impact on endometritis. In this study, an in vitro endometritis model was constructed using LPS. The expression levels of proinflammatory cytokines IL-6, IL-8, IL-1β, and TNF-α were significantly increased in the model, while the expression of bta-miR-25 was upregulated, and its target gene DUSP10 was downregulated. We further validated DUSP10 as a target gene of bta-miR-25 through a dual-luciferase reporter gene assay. Knockdown of bta-miR-25 can increase the decreased expression of DUSP10 levels and inhibited the increase in inflammatory factors induced by LPS. Subsequently, overexpression DUSP10 also inhibited the LPS-induced increase in inflammatory factors. In summary, bta-miR-25 can inhibit LPS-induced endometritis by over the expression of DUSP10. bta-miR-25 and DUSP10 may serve as biomarkers and potential therapeutic targets for endometritis in dairy cows.