Urolithin A Enhances the Development of Porcine Parthenogenetic Embryos by Promoting Mitochondrial Function and Quantity Through the SIRT1/PGC-1α Signaling Pathway.

Maintaining mitochondrial function and quantity is important for preimplantation embryo development, as they are essential for the regulation of oxidative stress. Urolithin A (UA), a metabolite produced from ellagitannins by gut bacteria, is known to exert antioxidant effects by improving mitochondrial function and biogenesis. Therefore, this study aimed to investigate the effects of UA on preimplantation embryo development and its mitochondrial function and quantity. In this study, EX-527, a specific inhibitor of sirtuin 1 (SIRT1), was used to explore whether the effects of UA are mediated by the SIRT1/peroxisome proliferator-activated receptor-co-activator 1α (PGC-1α) signaling pathway. UA significantly enhanced preimplantation development of porcine parthenotes. In addition, UA significantly increased mitochondrial function and quantity, intracellular glutathione levels, and the protein levels of SIRT1 and PGC-1α, whereas it reduced intracellular reactive oxygen species levels. Furthermore, the expression levels of SIRT1/PGC-1α signaling pathway- and mitochondrial biogenesis-related transcripts were significantly increased by UA treatment. However, the effects of UA were completely abolished by EX-527 cotreatment. These results suggest that UA improves preimplantation embryo development by enhancing mitochondrial function and quantity via the SIRT1/PGC-1α signaling pathway.