Effect of Chrysin on Gentamicin-induced Nephrotoxicity in Laboratory Animals

Background: Clinically Gentamicin (GM) is commonly used aminoglycoside antibiotic for the treatment of life-threatening Gram-negative bacterial infections, but the nephrotoxic potential of drug limit its clinical interest. Chrysin a plant flavonoid possess potent antioxidant and anti-inflammatory activity. Objective: To investigate the potential of chrysin against GM-induced nephrotoxicity. Materials and Methods: Nephrotoxicity was induced in male Sprague-Dawley rats (220-250 g) by intraperitoneal administration of gentamicin (120 mg kgG1) for 7 consecutive days. Rats were either treated with chrysin (10, 20 and 40 mg kgG1, p.o.) or methylprednisolone (12.5 mg kgG1, i.p.) or vehicle distilled water (10 mg kgG1, p.o.) for the 7 days. Various biochemical, molecular and histological parameters were assessed in serum and kidney. Results: The GM-administration significantly increased (p<0.001) the serum creatinine and Blood Urea Nitrogen (BUN) as well as renal malonaldehyde (MDA), Nitric Oxide (NO) along with renal Kidney Injury Molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) mRNA expressions. In addition, GM also significantly decreased (p<0.001) the renal superoxide dismutase (SOD), reduced glutathione (GSH) and mitochondrial enzymes (NADH dehydrogenase and cytochrome c oxidase) activities. However, rats treated with chrysin (10, 20 and 40 mg kgG1, p.o.) failed to produce any significant inhibition in altered levels of antioxidant, inflammatory, apoptosis, AKI markers and mitochondrial depleted enzymes. Histopathological abbreviations were also did not ameliorates by chrysin treatment. Conclusion: Chrysin failed to produce any significant protection against gentamycin-induced renal toxicity.