Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 김희선 | * |
dc.contributor.author | 임예현 | * |
dc.date.accessioned | 2023-07-31T16:31:09Z | - |
dc.date.available | 2023-07-31T16:31:09Z | - |
dc.date.issued | 2023 | * |
dc.identifier.issn | 2045-2322 | * |
dc.identifier.other | OAK-33575 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/265300 | - |
dc.description.abstract | Parkinson’s disease (PD) is an incurable movement disorder characterized by dopaminergic cell loss, neuroinflammation, and α-synuclein pathology. Herein, we investigated the therapeutic effects of necrosulfonamide (NSA), a specific inhibitor of mixed lineage kinase domain-like protein (MLKL), in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. MLKL is an executor of necroptosis, a programmed cell death pathway that causes inflammation. Repeated administration of NSA resulted in the recovery of impaired motor performance and dopaminergic degeneration. Furthermore, NSA inhibited the phosphorylation, ubiquitylation, and oligomerization of MLKL, all of which are associated with MLKL cell death-inducing activity in dopaminergic cells in the substantia nigra (SN). NSA also inhibited microglial activation and reactive astrogliosis as well as the MPTP-induced expression of proinflammatory molecules such as tumor necrosis factor-α, interleukin-1β, inducible nitric oxide synthase, and cystatin F. Furthermore, NSA inhibited α-synuclein oligomerization and phosphorylation in the SN of MPTP-treated mice by inhibiting the activity of glycogen synthase kinase 3β and matrix metalloproteinase-3. In conclusion, NSA has anti-necroptotic, anti-inflammatory, and anti-synucleinopathic effects on PD pathology. Therefore, NSA is a potential therapeutic candidate for PD. © 2023, The Author(s). | * |
dc.language | English | * |
dc.publisher | Nature Research | * |
dc.title | Necrosulfonamide exerts neuroprotective effect by inhibiting necroptosis, neuroinflammation, and α-synuclein oligomerization in a subacute MPTP mouse model of Parkinson’s disease | * |
dc.type | Article | * |
dc.relation.issue | 1 | * |
dc.relation.volume | 13 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | Scientific Reports | * |
dc.identifier.doi | 10.1038/s41598-023-35975-y | * |
dc.identifier.wosid | WOS:001001303600081 | * |
dc.identifier.scopusid | 2-s2.0-85160750955 | * |
dc.author.google | Leem | * |
dc.author.google | Yea-Hyun | * |
dc.author.google | Kim | * |
dc.author.google | Do-Yeon | * |
dc.author.google | Park | * |
dc.author.google | Jung-Eun | * |
dc.author.google | Hee-Sun | * |
dc.contributor.scopusid | 김희선(57191372551) | * |
dc.contributor.scopusid | 임예현(25422269100) | * |
dc.date.modifydate | 20240222143226 | * |