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Gentamicin is an effective aminoglycoside antibiotic drug but unfortunately up to 30% of gentamicin-treated patients may develop nephrotoxicity. Suggested mechanisms of gentamicininduced nephrotoxicity included inflammation and oxidative stress injury. Evening primrose oil (EPO) has anti-inflammatory and antioxidant effects. The aim of current study was to assess the possible renoprotective effect of EPO/vitamin E combination treatment on gentamicin-induced nephrotoxicity in rats. Additionally, to address the responsible mechanism(s) of this effect. Eighteen adult male albino Sprague-Dawley rats were equally and randomly divided into three groups; normal control, gentamicin control and EPO/vitamin E treated groups. Gentamicin control group and EPO/vitamin E treated group received IP gentamicin injections for 5 days (100 mg/kg). EPO/vitamin E treated group received EPO/vitamin E (10 g and 200 IU /kg/day respectively orally). Renal function, oxidative stress and histopathological changes were assessed. Renal tissue expressions of tumor necrosis factor α (TNF α) and nuclear Factor κβ (NFκβ) were assayed. Significant improvements of kidney function markers and tubular necrosis in EPO/vitamin E treated group were observed. EPO/vitamin E treatment significantly ameliorated the gentamicin-induced increase of renal lipid peroxidation and renal tissue expression of TNF α and NF-κβ. EPO/vitamin E treatment significantly ameliorated the gentamicin-induced decrease of renal glutathione and superoxide dismutase concentrations. Conclusion of current study is EPO/vitamin E combination treatment has renoprotective effect on gentamicin-induced nephrotoxicity by inhibiting renal TNF α /NF-κβ signaling pathway and the oxidative stress. Further researches for addressing the renoprotective effect of EPO treatment only and to determine other possible responsible mechanisms are needed

bulletin of egyptian society for physiological sciences

Evening Primrose Oil/ Vitamin E Combination Treatment Has Renoprotective Effect On Gentamicin-Induced Nephrotoxicity By Suppressing Renal Tumor Necrosis Factor α (TNF-α) / Nuclear Factor κβ (NF- κβ) Pathway And Inhibiting Renal Oxidative Stress