Activation of Nrf2 by ischemic preconditioning and sulforaphane in renal ischemia/reperfusion injury: a comparative experimental study.
Objective: The exposure of living creatures to drugs and chemicals often results in toxicity of liver and kidney. Drugs constitute an important and big part of the community and hospital-acquired kidney diseases. In this study, we investigated the effect of sulforaphane (SFN) on the levels of cystatin-C and lipid peroxidation on acetaminophen (APAP)induced nephrotoxicity in rats. Methods: Thirty-six Sprague-Dawley rats were separated equally into four experimental groups: control group, SFN group, APAP group, and APAP + SFN group. In the experimental treatment groups APAP was administered oral gavage at 1 g/kg 3 h after SFN treatment in last day and, in the APAP + SFN group, SFN was administered oral gavage at a dose of 500 μg/kg exactly for three days. Rats were euthanized and sacrificed 24 h after APAP administration. Results: APAP administration showed to significant increase in serum BUN, creatinine, urea and LDH concentrations as compared to the control datas indicating the induction of severe nephrotoxicity (p<0.001). SFN treatment significantly decreased the cystatin-C levels and lipid peroxidation compared to APAP group (p<0.05). Conclusion: The present study demonstrate that the attachment of SFN to the nephrotoxicity treatment protocol will be beneficial and further studies should be conducted for cystatin C which plays an important role in kidney toxicity and disease to be routinized as a biomarker.