effect of beta vulgaris and laurus nobitis on lipid profile and kidney in hyperuricemia rat

Hyperuricemia is a major contributor to various chronic and metabolic diseases. it contributes to hyperlipidemia, elevated serum creatinine, hyperglycemia, and weight gain through multiple pathways and mechanisms. this study aimed to investigate the effects of beta vulgaris and laurus nobilis on reducing the risk of hyperuricemia-related metabolic disorders and kidney damage in a rat model. twenty-four adult male albino rats (weighing approximately 200–220 g and aged 8–12 weeks) were housed in the animal facility. hyperuricemia was induced in the model group by administering oxonic acid (250 mg/kg body weight). treatment groups received either beta vulgaris or laurus nobilis following hyperuricemia induction. kidney tissue samples were examined histopathologically, and biochemical tests were conducted on all rat groups. in rats treated with laurus nobilis and beta vulgaris, all biochemical parameters—excluding hdl—were significantly decreased compared to the hyperuricemia model rats (p ≤ 0.01). notably, cholesterol (49.00±6.48), triglycerides (47.25±2.22), ldl (34.50±3.11), uric acid (4.90±0.22), urea (46.00±0.82), creatinine (0.35±0.03), blood glucose (193.00±11.20), and weight gain (77.75±2.06) were lower. histopathological analysis showed reduced nephron damage in rats treated with beta vulgaris and laurus nobilis. this study demonstrated that hyperuricemia induces kidney damage and metabolic disorders, including dyslipidemia, hyperglycemia, increased serum creatinine, urea, and weight gain in model rats. beta vulgaris and laurus nobilis significantly reduced these biochemical parameters and ameliorated histopathological signs of hyperuricemia, such as glomerular atrophy and hydropic changes in proximal tubular epithelial cells. laurus nobilis exerted a more substantial effect on lipid profile, blood glucose, serum creatinine, weight, and urea levels than beta vulgaris.