Uric acid sodium acts as a scavenger of oxygen radicals and plays a critical role as an antioxidant. It helps maintain blood pressure stability and manages oxidative stress. This compound effectively removes reactive oxygen species (ROS) such as singlet oxygen and peroxynitrite, thus inhibiting lipid peroxidation[1].[2].
体内研究
Uric acid, administered orally at a dose of 250 mg/kg, mitigates indomethacin-induced enteropathy[2].
Oral administration of uric acid decreased ROS accumulation in the ileum in a mouse model of indomethacin-induced enteropathy[2].
体外研究
In cellular experiments, Uric acid sodium at a concentration of 400 μM protects Caco-2 cells from lipid peroxidation caused by indomethacin over a 48-hour period[2].
When cells are co-treated with Indomethacin and Uric acid sodium (200 μM IND plus 400 μM UA for 24 hours), there is a significant reduction in ROS levels compared to cells treated with indomethacin alone. Additionally, cell viability in Caco-2 cells treated with both Indomethacin and Uric acid sodium is higher than in those treated only with indomethacin, indicating a protective effect against indomethacin-induced intestinal cell damage due to its antioxidant activity[2].
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