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Cited 13 time in webofscience Cited 15 time in scopus
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Nicotinamide Improves Functional Recovery via Regulation of the RAGE/JNK/NF-kappa B Signaling Pathway after Brain Injury

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dc.contributor.authorAlam, Sayed Ibrar-
dc.contributor.authorRehman, Shafiq Ur-
dc.contributor.authorKim, Myeong Ok-
dc.date.accessioned2022-12-26T15:16:04Z-
dc.date.available2022-12-26T15:16:04Z-
dc.date.created2022-12-13-
dc.date.issued2019-02-
dc.identifier.issn2077-0383-
dc.identifier.urihttps://scholarworks.bwise.kr/gnu/handle/sw.gnu/9486-
dc.description.abstractBrain injuries are a serious global health issue and are the leading cause of neurodegeneration. To date, there is no proper cure and treatment for brain-injury-induced neuropathological conditions because of a lack of sufficient knowledge and the failure to develop a drug due to the multi-pathological conditions in the brain. Herein, we explored the neurotherapeutic effects of Nicotinamide (NAM), against brain injury-induced neurodegeneration and behavioral problems. Treating injured mouse brains with NAM, for 7 days, significantly ameliorated several pathological events. Interestingly, NAM treatment significantly inhibited the injury-induced activation of receptor for advanced glycation end-products (RAGE), c-Jun N-terminal kinases (JNK), and neuroinflammatory mediators, such as NF-kappa B, TNF-alpha, IL-1 beta, and NOS2 in the brain, and it also regulated the levels of apoptotic markers, including Bax, caspase-3, and Bcl-2. Furthermore, treatment using NAM in TBI mice, significantly reversed synaptic protein loss and improved memory impairments and behavioral outcomes. Our findings suggested that NAM treatment reduced injury-induced secondary neurodegenerative pathology by modulating RAGE/JNK/NF-kappa B signaling in mice. Therefore, we recommend that NAM would be a safe and efficient therapeutic agent against brain-injury-induced neurodegeneration.-
dc.language영어-
dc.language.isoen-
dc.publisherMDPI-
dc.subjectOXIDATIVE STRESS-
dc.subjectMITOCHONDRIAL DYSFUNCTION-
dc.subjectCOGNITIVE IMPAIRMENT-
dc.subjectALZHEIMERS-DISEASE-
dc.subjectBETA PEPTIDE-
dc.subjectHEAD-INJURY-
dc.subjectCELL-DEATH-
dc.subjectNEUROINFLAMMATION-
dc.subjectRAGE-
dc.subjectACTIVATION-
dc.titleNicotinamide Improves Functional Recovery via Regulation of the RAGE/JNK/NF-kappa B Signaling Pathway after Brain Injury-
dc.typeArticle-
dc.contributor.affiliatedAuthorKim, Myeong Ok-
dc.identifier.doi10.3390/jcm8020271-
dc.identifier.scopusid2-s2.0-85064039257-
dc.identifier.wosid000460295400144-
dc.identifier.bibliographicCitationJOURNAL OF CLINICAL MEDICINE, v.8, no.2-
dc.relation.isPartOfJOURNAL OF CLINICAL MEDICINE-
dc.citation.titleJOURNAL OF CLINICAL MEDICINE-
dc.citation.volume8-
dc.citation.number2-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaGeneral & Internal Medicine-
dc.relation.journalWebOfScienceCategoryMedicine, General & Internal-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusMITOCHONDRIAL DYSFUNCTION-
dc.subject.keywordPlusCOGNITIVE IMPAIRMENT-
dc.subject.keywordPlusALZHEIMERS-DISEASE-
dc.subject.keywordPlusBETA PEPTIDE-
dc.subject.keywordPlusHEAD-INJURY-
dc.subject.keywordPlusCELL-DEATH-
dc.subject.keywordPlusNEUROINFLAMMATION-
dc.subject.keywordPlusRAGE-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordAuthorbrain injury-
dc.subject.keywordAuthornicotinamide-
dc.subject.keywordAuthorneurodegeneration-
dc.subject.keywordAuthorsynaptic dysfunction-
dc.subject.keywordAuthorneuroinflammation-
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