2017 年 10 巻 4 号 p. 417-422
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<0.01); the PAS-positive area in the edaravone group remained comparable to that in the normal group (52.9±0.9%, P<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/mm2, P<0.01), while they were significantly reduced in the edaravone group (32.8±5.7 cells/mm2, P<0.01).
Conclusion: Edaravone pretreatment mitigates MNMS-induced kidney damage by reducing both glycogen depletion and neutrophil infiltration.
