4,5-dianilinophtalimide protects neuroendocrine cells against serum deprivation-induced stress and apoptosis

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dc.citation.epage365en_US
dc.citation.issueNumber5en_US
dc.citation.spage359en_US
dc.citation.volumeNumber34en_US
dc.contributor.authorErgin V.en_US
dc.contributor.authorErdogan, M.en_US
dc.contributor.authorKarasu Ç.en_US
dc.contributor.authorMenevşe, A.en_US
dc.date.accessioned2016-02-08T09:34:47Z
dc.date.available2016-02-08T09:34:47Z
dc.date.issued2013en_US
dc.departmentInstitute of Materials Science and Nanotechnology (UNAM)en_US
dc.description.abstractOBJECTIVE: The aim of this study was to reveal the effects of 4,5-dianilinophthalimide (DAPH), which inhibits amyloid β fibrillization, against serum deprivation (SD)-induced apoptosis and the possible mechanisms in differentiated PC12 neuron cells. METHODS: Firstly, we evaluated whether DAPH protects cell viability exposed to SD by MTT assay. Next, we examined the changes of phospho-p38 MAPK (Thr180/Tyr182), phospho-HSP27 (Ser82), phospho-c-JUN (Ser73) and cleaved-CASP3 (Asp175) profiles by immunoblotting, in PC12 cells exposed to SD. Intracellular reactive oxygen species (ROS) level was also measured. RESULTS: SD induced apoptosis accompanied by up-regulation of phospho-p38 MAPK (Thr180/Tyr182), phospho-HSP27 (Ser82), phospho-c-JUN (Ser73), cleaved-CASP3 (Asp175) and intracellular ROS content. Co-treatment with nontoxic doses of DAPH prevented apoptosis by the attenuation of activated proteins and reduction of ROS level. These results suggest that serum deprivation-induced apoptosis inhibited by DAPH administration. CONCLUSION: We have provided for the first evidence that DAPH has a neuroprotective effect on SD-caused stress, probably via contributing the reestablishment of redox homeostasis. © 2013 Neuroendocrinology Letters.en_US
dc.identifier.issn0172780X
dc.identifier.urihttp://hdl.handle.net/11693/20765
dc.language.isoEnglishen_US
dc.source.titleNeuroendocrinology Lettersen_US
dc.subjectApoptosisen_US
dc.subjectCellular stressen_US
dc.subjectDAPHen_US
dc.subjectPC12en_US
dc.subjectSerum deprivationen_US
dc.subject4,5 dianilinophtalimideen_US
dc.subjectcaspase 3en_US
dc.subjectheat shock protein 27en_US
dc.subjectmitogen activated protein kinase p38en_US
dc.subjectneuroprotective agenten_US
dc.subjectprotein c junen_US
dc.subjectreactive oxygen metaboliteen_US
dc.subjectunclassified drugen_US
dc.subjectapoptosisen_US
dc.subjectarticleen_US
dc.subjectattenuationen_US
dc.subjectcell viabilityen_US
dc.subjectdrug effecten_US
dc.subjectimmunoblottingen_US
dc.subjectneuroprotectionen_US
dc.subjectneurosecretory cellen_US
dc.subjectoxidative stressen_US
dc.subjectPC12 cellen_US
dc.subjectserum deprivation induced apoptosisen_US
dc.subjectserum deprivation induced stressen_US
dc.subjectupregulationen_US
dc.subjectAnimalsen_US
dc.subjectApoptosisen_US
dc.subjectCaspase 3en_US
dc.subjectCell Survivalen_US
dc.subjectHSP27 Heat-Shock Proteinsen_US
dc.subjectNeuronsen_US
dc.subjectNeuroprotective Agentsen_US
dc.subjectp38 Mitogen-Activated Protein Kinasesen_US
dc.subjectPC12 Cellsen_US
dc.subjectPhosphorylationen_US
dc.subjectPhthalimidesen_US
dc.subjectProto-Oncogene Proteins c-junen_US
dc.subjectRatsen_US
dc.subjectReactive Oxygen Speciesen_US
dc.subjectStress, Physiologicalen_US
dc.subjectUp-Regulationen_US
dc.title4,5-dianilinophtalimide protects neuroendocrine cells against serum deprivation-induced stress and apoptosisen_US
dc.typeArticleen_US
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Institute of Materials Science and Nanotechnology (UNAM)