Abstract
The present study was carried out to evaluate the renoprotective antioxidant effect of Spirulina platensis on gentamicin-induced acute tubular necrosis in rats. Albino-Wistar rats, (9male and 9 female), weighing approximately 250 g, were used for this study. Rats were randomly assigned to three equal groups. Control group received 0,9 % sodium chloride intraperitoneally for 7 days at the same volume as gentamicin group. Gentamicin group was treated intraperitoneally with gentamicin, 80 mg/kg daily for 7 days. Gentamicin+spirulina group received Spirulina platensis 1000 mg/kg orally 2 days before and 7 days concurrently with gentamicin (80 mg/kg i.p.). Nephrotoxicity was assessed by measuring plasma nitrite concentration, stabile metabolic product of nitric oxide with oxygen. Plasma nitrite concentration was determined by colorimetric method using Griess reaction. For histological analysis kidney specimens were stained with hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) stain. Plasma nitrite concentration and the level of kidney damage were significantly higher in gentamicin group in comparison both to the control and gentamicin+spirulina group. Spirulina platensis significantly lowered the plasma nitrite level and attenuated histomorphological changes related to renal injury caused by gentamicin. Thus, the results from present study suggest that Spirulina platensis has renoprotective potential in gentamicin-induced acute tubular necrosis possibly due to its antioxidant properties.
Highlights
The aminoglycoside antibiotic is very effective in treating gram-negative infections ( )
No significant difference was found between control and gentamicin+spirulina group (p=, ) (Figure .)
For a more overall insight in pathophysiological mechanisms in the development of toxic tubular damage induced with gentamicin, as well as in new therapeutic approach, numerous studies were conducted in experimental model of acute tubular necrosis (ATN) (, )
Summary
The aminoglycoside antibiotic (gentamicin) is very effective in treating gram-negative infections ( ). Acute renal failure is major complication in - of patients receiving the drug ( ). It has been demonstrated that gentamicin-induced nephrotoxicity is characterized by direct tubular necrosis, which is localized mainly in proximal tubules ( ). The exact mechanisms of gentamicin-induced nephrotoxicity still remain unclear. Recent evidence showed that reactive oxygen species (ROS) play a pivotal role in gentamicinmediated nephrotoxicity. Walker et al ( ) have demonstrated that oxidative stress induced by gentamicin, is the central pathway responsible for renal injury. Some studies have reported that antioxidant administration ameliorates gentamicin-induced nephropathy ( )
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