role of antioxidant and anti-inflammatory parameters in the renoprotective effects of valsartan against renal ischemia-reperfusion injury in male rats

Renal ischemia–reperfusion (i/r) injury, a major cause of acute kidney injury, is characterized by inflammation, oxidative stress, and functional impairment. valsartan, an angiotensin ii receptor blocker, reduces blood pressure and exhibits anti-inflammatory and antioxidant properties. this study evaluated the renoprotective effects of valsartan through antioxidant and anti-inflammatory parameters in a male rat model of renal i/r. eighteen male wistar rats (250–300 g) were randomly assigned to three groups: sham control, i/r control, and i/r treated with valsartan. valsartan (60 mg/kg) was administered orally by gavage for one week before and immediately after i/r induction. after 24 hours, urine, blood, and kidney tissue samples were collected to assess biochemical and functional parameters including mean arterial pressure (map), inflammatory and oxidative stress markers, and histopathological alterations. in the i/r group, blood urea nitrogen (bun), tumor necrosis factor-alpha (tnf-α), tissue malondialdehyde (mda), fractional excretion of sodium (fena) and potassium (fek), urinary sodium, and plasma creatinine significantly increased, while glomerular filtration rate (gfr), ferric reducing antioxidant power (frap), superoxide dismutase (sod), catalase (cat), glutathione peroxidase (gpx), and map significantly decreased (p<0.05). valsartan treatment significantly reduced urinary urea, bun, tnf-α, and fena, improved antioxidant enzyme activities and plasma frap, and increased urinary creatinine, potassium, and sodium compared with the i/r group (p<0.05). histopathological examination demonstrated reduced renal tissue injury following valsartan treatment. overall, valsartan attenuated renal i/r injury by reducing oxidative stress, inflammation, and structural damage, suggesting potential therapeutic benefits that warrant further clinical investigation.