2005
DOI: 10.1016/j.urology.2005.04.035
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Edaravone protects against ischemia/reperfusion-induced functional and biochemical changes in rat urinary bladder

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Cited by 28 publications
(22 citation statements)
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“…In rats, edaravone was reported to protect the contractile responses to field stimulation and carbachol, as well as reduce MDA content following I/R-induced damage to the bladder (83).…”
Section: Bladder Injurymentioning
confidence: 99%
“…In rats, edaravone was reported to protect the contractile responses to field stimulation and carbachol, as well as reduce MDA content following I/R-induced damage to the bladder (83).…”
Section: Bladder Injurymentioning
confidence: 99%
“…CP-induced cystitis is caused by the metabolite acrolein, which rapidly enters into the urothelial cells and produces ROS, and is prevented by ROS scavengers or antioxidants (13, 20 -22). It is suggested that bladder dysfunction induced by bladder outlet obstruction (23,24) and ischemia/reperfusion (25,26) are due to the generation of ROS. In addition, ROS are abundantly produced by infiltrated inflammatory cells such as macrophages, neutrophils, and mast cells in the inflamed bladder (27 -29).…”
mentioning
confidence: 99%
“…Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-1; norphenazone; MCI-186), a potent scavenger of hydroxyl and peroxyl radicals, inhibits lipid peroxidation via its antioxidant activity. Animal studies on the mitigation of small intestine damage found that edaravone decreases the degree of I-R-mediated mucosal tissue injury [5][6][7]. Elsewhere, we showed that, in a rabbit ASMAT model that introduced autologous fibrin clots, thrombolysis via the intra-arterial administration of edaravone and urokinase contributed to a reduction in the degree of I-R injury to the small intestinal mucosa [4].…”
mentioning
confidence: 57%