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Raloxifene attenuates oxidative stress and preserves mitochondrial function in astrocytic cells upon glucose deprivation

dc.contributor.authorVesga-Jiménez D.J.
dc.contributor.authorHidalgo-Lanussa O.
dc.contributor.authorBaez-Jurado E.
dc.contributor.authorEcheverria V.
dc.contributor.authorAshraf G.M.
dc.contributor.authorSahebkar A.
dc.contributor.authorBarreto G.E.
dc.date.accessioned2020-09-02T22:30:01Z
dc.date.available2020-09-02T22:30:01Z
dc.date.issued2019
dc.identifier10.1002/jcp.27481
dc.identifier.citation234, 3, 2051-2057
dc.identifier.issn00219541
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6552
dc.descriptionOxidative stress and mitochondrial dysfunction induced by metabolic insults are both hallmarks of various neurological disorders, whereby neuronal cells are severely affected by decreased glucose supply to the brain. Likely injured, astrocytes are important for neuronal homeostasis and therapeutic strategies should be directed towards improving astrocytic functions to improve brain's outcome. In the present study, we aimed to assess the actions of raloxifene, a selective estrogen receptor modulator in astrocytic cells under glucose deprivation. Our findings indicated that pretreatment with 1 µM raloxifene results in an increase in cell viability and attenuated nuclei fragmentation. Raloxifene's actions also rely on the reduction of oxidative stress and preservation of mitochondrial function in glucose-deprived astrocytic cells, suggesting the possible direct effects of this compound on mitochondria. In conclusion, our results demonstrate that raloxifene's protective actions might be mediated in part by astrocytes in the setting of a metabolic insult. © 2018 Wiley Periodicals, Inc.
dc.language.isoen
dc.publisherWiley-Liss Inc.
dc.subjectastrocytes
dc.subjectglucose deprivation
dc.subjectmitochondria
dc.subjectneuroprotection
dc.subjectraloxifene
dc.subjectcardiolipin
dc.subjectglucose
dc.subjecthydrogen peroxide
dc.subjectraloxifene
dc.subjectreactive oxygen metabolite
dc.subjectsuperoxide
dc.subjectcardiolipin
dc.subjectglucose
dc.subjectneuroprotective agent
dc.subjectprotective agent
dc.subjectraloxifene
dc.subjectreactive oxygen metabolite
dc.subjectselective estrogen receptor modulator
dc.subjectArticle
dc.subjectastrocyte
dc.subjectastrocyte cell line
dc.subjectbrain mitochondrion
dc.subjectcell nucleus
dc.subjectcell survival
dc.subjectcell viability
dc.subjectconcentration response
dc.subjectmitochondrial membrane potential
dc.subjectMTT assay
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectastrocyte
dc.subjectcell line
dc.subjectcytology
dc.subjectdrug effect
dc.subjecthuman
dc.subjectmetabolism
dc.subjectmitochondrion
dc.subjectoxidative stress
dc.subjectAstrocytes
dc.subjectCardiolipins
dc.subjectCell Line
dc.subjectCell Survival
dc.subjectGlucose
dc.subjectHumans
dc.subjectMembrane Potential, Mitochondrial
dc.subjectMitochondria
dc.subjectNeuroprotective Agents
dc.subjectOxidative Stress
dc.subjectProtective Agents
dc.subjectRaloxifene Hydrochloride
dc.subjectReactive Oxygen Species
dc.subjectSelective Estrogen Receptor Modulators
dc.titleRaloxifene attenuates oxidative stress and preserves mitochondrial function in astrocytic cells upon glucose deprivation
dc.typeArticle


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