Kiyoshi KikuchiSalunya TancharoenFumiyo MatsudaKamal Krishna BiswasTakashi ItoYoko MorimotoYoko OyamaKazunori TakenouchiNaoki MiuraNoboru ArimuraYuko NawaXiaojie MengBinita ShresthaShinichiro ArimuraMasahiro IwataKentaro MeraHisayo SameshimaYoshiko OhnoRyuichi MaenosonoYutaka TajimaHisaaki UchikadoTerukazu KuramotoKenji NakayamaMinoru ShigemoriYoshihiro YoshidaTeruto HashiguchiIkuro MaruyamaKo ichi KawaharaDivision of Laboratory and Vascular MedicineOmuta City General HospitalMahidol UniversityFaculty of MedicineKagoshima University Faculty of MedicineFaculty of AgricultureKurume University School of Medicine2018-09-132018-09-132009-12-25Biochemical and Biophysical Research Communications. Vol.390, No.4 (2009), 1121-1125109021040006291X2-s2.0-70549090013https://repository.li.mahidol.ac.th/handle/20.500.14594/27094Aquaporin-4 (AQP4) plays a role in the generation of post-ischemic edema. Pharmacological modulation of AQP4 function may thus provide a novel therapeutic strategy for the treatment of stroke, tumor-associated edema, epilepsy, traumatic brain injury, and other disorders of the central nervous system (CNS) associated with altered brain water balance. Edaravone, a free radical scavenger, is used for the treatment of acute ischemic stroke (AIS) in Japan. In this study, edaravone significantly reduced the infarct area and improved the neurological deficit scores at 24 h after reperfusion in a rat transient focal ischemia model. Furthermore, edaravone markedly reduced AQP4 immunoreactivity and protein levels in the cerebral infarct area. In light of observations that edaravone specifically inhibited AQP4 in a rat transient focal ischemia model, we propose that edaravone might reduce cerebral edema through the inhibition of AQP4 expression following cerebral infarction. © 2009 Elsevier Inc. All rights reserved.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.1016/j.bbrc.2009.09.015