Uric acid sodium is a potent and widely recognized antioxidant with the ability to scavenge oxygen free radicals, helping to maintain blood pressure stability and counteract oxidative stress. It effectively eliminates reactive oxygen species (ROS), such as singlet oxygen and peroxynitrite, and inhibits lipid peroxidation. Additionally, uric acid sodium is closely associated with the pathogenesis of gouty arthritis and the formation of calcium oxalate stones, and it can be used to induce hypertension models.

Uric acid, when administered at a concentration of 400 μM for 48 hours, offers protection to Caco-2 cells by preventing indomethacin-induced lipid peroxidation [2]. Furthermore, co-treatment of cells with indomethacin and uric acid sodium (200 μM indomethacin plus 400 μM uric acid; 24 hours) significantly reduces reactive oxygen species (ROS) levels compared to cells treated with indomethacin alone. Additionally, cell viability in Caco-2 cells exposed to both indomethacin and uric acid sodium (200 μM indomethacin plus 400 μM uric acid; 24 hours) is higher compared to cells treated solely with indomethacin. The protective effect of uric acid sodium on indomethacin-induced changes in intestinal cells is attributed to its antioxidant activity [2].

Oral treatment of uric acid sodium at a dosage of 250 mg/kg has a beneficial effect on indomethacin-induced enteropathy. It ameliorates the enteropathy caused by indomethacin. Oral treatment of uric acid sodium leads to a reduction in ROS accumulation in the ileum in a mouse model of indomethacin-induced enteropathy [2].

DMSO: 2.8 mg/mL (14.73 mM), when pH is adjusted to 4 with HCl. Sonication and heating to 60℃ are recommended.