Uric acid sodium, scavengers of oxygen radicals, is a potent and common antioxidant that helps maintain stable blood pressure and resist oxidative stress. Uric acid sodium, which removes reactive oxygen species (ROS) such as singlet oxygen and peroxynitrite, has an inhibitory effect on lipid peroxidation and is associated with the pathogenesis of gout joint disease and the formation of calcium oxalate stones.

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].