Abstract

Objective To explore mechanism and protective effect of dexamethasone on renal injury induced by ischemia-reperfusion in rats. Methods The right kidney of rats was excised and the left renal artery was clamped with non-invasive clamp for 60 minutes to replicate the renal ischemia-reperfusion model. The successful rats were divided into model group and dexamethasone group (10 mg/kg). At the same time, the sham operation group was established (right kidney was not resected, left renal artery was not clamped). There were 10 rats in each group. Rats were scored for renal tubular injury. The level of malondialdehyde (MDA), the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), the level of tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6, and the expression of nuclear factor-κ-gene binding κ (NF-κB) signal pathway related protein was detected. The variance analysis and LSD-t test are used in the data analysis. Results Compared with the model group, the renal tubular injury score [(41.56±4.16) vs. (85.32±8.53)] was decreased (t=14.580, P<0.01), the contents of TNF-α [(4.56±0.48) vs. (14.23±1.42)], IL-1β [(72.47±7.25) vs. (243.56±24.53)], IL-6 [(98.24±9.82) vs. (232.38±20.68)] and MDA [(47.34±4.73) vs. (84.24±8.42)] was decreased (t=20.400, P<0.01), the activities of SOD [(4.36±0.44) vs. (2.74±0.27)], CAT [(10.24±1.36) vs. (8.69±0.87)] and GSH-Px [(18.62±1.87) vs. (14.53±1.43)] was increased (t=9.920, P<0.01), and the expressions of p-IκBα [(0.42±0.03) vs. (0.98±0.10)] and p-NF-κB p65 [(0.39±0.04) vs. (1.95±0.15)] was decreased in dexamethasone group (t=16.960, P<0.01). Conclusion Dexamethasone might inhibit renal ischemia-reperfusion injury in rats through antioxidant and anti-inflammatory effects. Key words: Dexamethasone; Ischemia-reperfusion; Renal injury; Oxidant; Inflammation

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.