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dc.contributor.authorWilasinee Suwanjangen_US
dc.contributor.authorKay L.H. Wuen_US
dc.contributor.authorSupaluk Prachayasittikulen_US
dc.contributor.authorBanthit Chetsawangen_US
dc.contributor.authorKomgrid Charngkaewen_US
dc.contributor.otherChang Gung Memorial Hospitalen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherFaculty of Medicine, Siriraj Hospital, Mahidol Universityen_US
dc.identifier.citationNeurochemical Research. (2019)en_US
dc.description.abstract© 2019, Springer Science+Business Media, LLC, part of Springer Nature. Dexamethasone is an approved steroid for clinical use to activate or suppress cytokines, chemokines, inflammatory enzymes and adhesion molecules. It enters the brain, by-passing the blood brain barrier, and acts through genomic mechanisms. High levels of dexamethasone are able to induce neuronal cell loss, reduce neurogenesis and cause neuronal dysfunction. The exact mechanisms of steroid, especially the dexamethasone contribute to neuronal damage remain unclear. Therefore, the present study explored the mitochondrial dynamics underlying dexamethasone-induced toxicity of human neuroblastoma SH-SY5Y cells. Neuronal cells treatment with the dexamethasone resulted in a marked decrease in cell proliferation. Dexamethasone-induced neurotoxicity also caused upregulation of mitochondrial fusion and cleaved caspase-3 proteins expression. Mitochondria fusion was found in large proportions of dexamethasone-treated cells. These results suggest that dexamethasone-induced hyperfused mitochondrial structures are associated with a caspase-dependent death process in dexamethasone-induced neurotoxicity. These findings point to the high dosage of dexamethasone as being neurotoxic through impairment of mitochondrial dynamics.en_US
dc.rightsMahidol Universityen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleMitochondrial Dynamics Impairment in Dexamethasone-Treated Neuronal Cellsen_US
Appears in Collections:Scopus 2019

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