Abstract
BackgroundAcute renal failure may complicate ischemic‐reperfusion injury (IRI) due to the production of reactive oxygen species. Atorvastatin (ATO) is well known for its antioxidant and antiinflammatory effects. It may be possible to protect against acute renal failure by preventing IRI.Aim of studyThe current study has been carried out to investigate the protective effect of ATO against renal IRI in diabetic rats.MethodsThe current study used 2 groups of rats, A and B, (18 rats each). Group A (non‐diabetic) was subdivided into: Group A1 (non‐diabetic sham), Group A2 (non‐diabetic IRI), Group A3 (non‐diabetic ATO‐treated + IRI). Group B (diabetic) was subdivided into: Group B1 (diabetic sham), Group B2 (diabetic IRI), and Group B3 (diabetic ATO‐treated + IRI). All rats were subjected to renal ischemia, bilaterally, for 45 minutes, followed by reperfusion for 24 hours. Rats in Groups A3 and B3 were injected with single doses of ATO (10 mg/kg), intraperitoneal, half hour before induction of renal ischemia. Serum kidney functions including blood urea nitrogen (BUN) and creatinine, and oxidative stress markers in renal tissue homogenate, including malondialdehyde (MDA), inducible nitric oxide synthase (iNOS), superoxide dismutase (SOD), and glutathione reductase (GR), were studied to measure renal IRI.ResultsGroups A2 and B2 revealed marked increase in BUN, creatinine, MDA, and iNOS and a decrease in SOD and GR. Corresponding results in Groups A3 and B3 suggested improvement in both, the kidney function tests and the oxidative stress markers. This improvement was more significant in Group A3 than Group B3. Study data were analyzed using SPSS and data were described as mean ± standard deviation (SD). Comparisons were performed using one‐way analysis of variance. Differences between mean values were assessed using a t test. A P<.05 was considered statistically significant.ConclusionATO can improve renal IRI, both, in non‐diabetic and diabetic rats, however, its protective effect was less in diabetic rats.Support or Funding InformationThis study was self‐funded.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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