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Rania G. Abdel-latif,Rehab A. Rifaai,Entesar F. Amin 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.5
Ischemic stroke is a serious condition associatedwith severe functional disability and high mortality,however; eff ective therapy remains elusive. Empaglifl ozin,a sodium-glucose cotransporter 2 inhibitor, has been shownto exert additional non-glycemic benefi ts including antiapoptoticeff ects in diff erent disease settings. Thereby, thisstudy was designed to investigate the ameliorative eff ect ofempaglifl ozin on the neuronal apoptosis exhibited in cerebralischemia/reperfusion (I/R) in a rat model targetingHIF-1α/VEGF signaling which is involved in this insult. Global cerebral I/R injury was induced in male Wistar ratsthrough occlusion of the bilateral common carotid arteriesfor 30 min followed by one-hour reperfusion. Empaglifl ozindoses of 1 and 10 mg/kg were administered 1 and 24 h afterreperfusion. In I/R-injured rats, empaglifl ozin treatmentssignifi cantly reduced infarct size and enhanced neurobehavioralfunctions in a dose-dependent manner. The drugalleviated neuronal death and cerebral injury infl icted byglobal ischemia as it suppressed neuronal caspase-3 proteinexpression. In parallel, protein expressions of HIF-1αand its downstream mediator VEGF were upregulated inthe ischemic brain following empaglifl ozin treatment. Theresults indicated that empaglifl ozin attenuates cerebral I/Rinducedneuronal death via the HIF-1α/VEGF cascade.