Gentamicin is a widely used
antibiotic against serious and life-threatening
infections; however, its usefulness is limited by the development of nephrotoxicity. The present study was designed to determine whether
flavocoxid has a protective effect against
gentamicin-induced nephrotoxicity in rats. For this purpose, we quantitatively evaluated
gentamicin-induced renal structural and functional alterations using histopathological and biochemical approaches. Furthermore, the effect of
flavocoxid on
gentamicin induced
hypersensitivity of urinary bladder rings to
acetylcholine (ACh) was determined. Twenty-four male Wistar albino rats were randomly divided into three groups, namely control,
gentamicin (100 mg/kg, i.p.) and
gentamicin plus
flavocoxid (20 mg/kg, orally). At the end of the study, all rats were sacrificed and then blood, urine samples and kidneys were collected for further analysis.
Gentamicin administration caused a severe nephrotoxicity which was evidenced by an elevated renal somatic index (RSI), serum
creatinine, blood
urea nitrogen, serum
lactate dehydrogenase, and
protein in urine with a concomitant reduction in
serum albumin and normalized
creatinine clearance value as compared with the controls. Moreover, a significant increase in renal contents of
malondialdehyde,
myeloperoxidase, and
tumor necrosis factor-alpha with a significant decrease in renal
reduced glutathione and
superoxide dismutase activities was detected upon
gentamicin administration together with increasing the sensitivity of isolated urinary bladder rings to ACh. Exposure to
gentamicin induced
necrosis of renal tubular epithelial cells.
Flavocoxid protected kidney tissue against the oxidative damage and the nephrotoxic effect caused by
gentamicin treatment. In addition,
flavocoxid significantly reduced the responses of isolated bladder rings to ACh. The results from our study indicate that
flavocoxid supplement attenuates
gentamicin-induced renal injury via the amelioration of oxidative stress and
inflammation of renal tubular cells.