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Objective : We have previously shown that pretreatment with the free radical scavenger edaravone (Radicut ® , Mitsubishi Tanabe Pharma Co., Japan) mitigated skeletal muscle damage due to ischemia reperfusion. In this study, we sought to validate its use in an experimental model of myonephropathic-metabolic syndrome (MNMS). Methods : Either edaravone (3.0 mg/kg; edaravone group; n=4) or saline (saline group; n=6) was intraperitoneally injected into male Lewis rats (508±31 g). Normal kidneys were harvested as control (n=3). MNMS was induced by bilaterally clamping the common femoral arteries for 5 h and declamping 5 h later. Kidney damage was evaluated by quantifying Periodic Acid Schiff (PAS)-positive area (glycogen storage) and esterase-positive cells (neutrophil infiltration). Results : The PAS-positive area in the saline group was significantly lower than that in the normal group (36.9±2.6 vs. 66.9±1.2%, P&lt;0.01); the PAS-positive area in the edaravone group remained comparable to that in the normal group (52.9±0.9%, P&lt;0.01). Esterase-positive cells in the saline group were significantly higher than in normal kidneys (62.4±5.6 vs. 17.5±2.4 cells/mm 2 , P&lt;0.01), while they were significantly reduced in the edaravone group (32.8±5.7 cells/mm 2 , P&lt;0.01). Conclusion : Edaravone pretreatment mitigates MNMS-induced kidney damage by reducing both glycogen depletion and neutrophil infiltration.

annals of vascular diseases/avd

Pretreatment with the Free Radical Scavenger Edaravone Mitigates Kidney Glycogen Depletion and Neutrophil Infiltration after Leg Ischemia in a Rat Model: A Pilot Study