Document Type : Original Research Article
Department of Exercise Physiology, Faculty of Sport Science, University of Mazandaran, Babolsar, Iran,
Department of Physiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
Department of Exercise Physiology, Faculty of Sport Science, University of Mazandaran, Babolsar, I.R. Iran
Biochemistry, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
Objective: Ginger has protective effects on the kidney, however the molecular mechanism of this effect has not yet been fully elucidated. Therefore, this work studied molecular mechanisms of ginger effects on ethanol-induced kidney injury.
Materials and Methods: Twenty-four male Sprague-Dawley rats were randomly divided into four groups: control, ginger (1 g/kg/day ginger extract by oral gavage), ethanol (4 g/kg/day ethanol by oral gavage) and ginger-ethanol group and treated daily for 28 days. Kidney function, expression of nuclear factor erythroid 2-related factor 2 (NRF2) and tumor necrosis factor (TNF)-α genes and oxidative stress parameters in kidney tissue, were evaluated. Total phenolic content (TPC) and 2, 2-diphenyl-1-picrylhydrazyl (DPPH) scavenging activity of ginger extract were also evaluated.
Results: Hydroethanolic extract of ginger showed a good level of DPPH scavenging activity and TPC. In the ethanol group, serum level of urea, creatinine and uric acid and the expression of NRF2 and TNF-α significantly increased compared to control group, while co-treatment with ginger in ginger+ethanol group significantly ameliorated them compared to the ethanol group. Ethanol exposure significantly reduced the activity of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) compared to the control values ,while the level of malondialdehyde (MDA) significantly increased. Ginger significantly ameliorated the level of MDA and activity of SOD, GPx and CAT in the ginger-ethanol group compared to the ethanol group.
Conclusion: The results showed that ginger's protective effects against ethanol renotoxicity were mediated via enhancing the NRF2 and TNF-α expression.