β-Carboline alkaloid harmaline alleviates hyperuricemia-mediated renal inflammation by suppressing oxidative stress.

Hyperuricemia is a metabolic disorder marked by elevated serum uric acid levels and is closely linked to the development of gout and progressive renal dysfunction. It is increasingly recognized as a major public health concern due to its association with chronic kidney disease and cardiovascular complications. Hyperuricemia induces kidney impairment through a complex interplay of oxidative and inflammatory stress. Harmaline, a β-carboline alkaloid primarily found in Peganum harmala, exhibits antioxidant and anti-inflammatory activities. Considering the roles of oxidative and inflammatory stress in renal dysfunction and the modulatory potential of harmaline, this study aimed to evaluate harmaline against potassium oxonate-induced hyperuricemia and renal impairment in mice. In this study, 25 Swiss albino mice were divided into five groups (n = 5). Hyperuricemia was induced by intraperitoneal administration of potassium oxonate (300 mg/kg) for 7 days. Harmaline (2.5 and 5 mg/kg, i.p.) and allopurinol (10 mg/kg, i.p.) were administered 1-h after potassium oxonate treatment. On day 8, serum was collected to measure uric acid, creatinine, and blood urea nitrogen (BUN), and thereafter, the kidneys were harvested for biochemical analyses. Potassium oxonate administration resulted in hyperuricemia-associated renal dysfunction, as evidenced by increased serum uric acid, creatinine, BUN, thiobarbituric acid (TBARS), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6), along with decreased renal glutathione (GSH) and interleukin-10 (IL-10) levels. Treatment with harmaline significantly attenuated these potassium oxonate-induced biochemical and inflammatory alterations. Notably, the higher dose of harmaline exhibited the prominent effect. Overall, the results suggest that harmaline, particularly at 5 mg/kg, effectively alleviates potassium oxonate-induced hyperuricemia and renal dysfunction in mice.