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dc.contributor.author이지희*
dc.contributor.author김희선*
dc.contributor.author박진선*
dc.contributor.author임예현*
dc.date.accessioned2022-06-02T16:31:12Z-
dc.date.available2022-06-02T16:31:12Z-
dc.date.issued2022*
dc.identifier.issn1661-6596*
dc.identifier.otherOAK-31411*
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/261248-
dc.description.abstractNeuroinflammation is crucial in the progression of neurodegenerative diseases. Thus, con-trolling neuroinflammation has been proposed as an important therapeutic strategy for neurodegener-ative disease. In the present study, we examined the anti-inflammatory and neuroprotective effects of GTS-21, a selective α7 nicotinic acetylcholine receptor (α7 nAChR) agonist, in neuroinflammation and Parkinson’s disease (PD) mouse models. GTS-21 inhibited the expression of inducible nitric oxide syn-thase (iNOS) and proinflammatory cytokines in lipopolysaccharide (LPS)-stimulated BV2 microglial cells and primary microglia. Further research revealed that GTS-21 has anti-inflammatory properties by inhibiting PI3K/Akt, NF-κB, and upregulating AMPK, Nrf2, CREB, and PPARγ signals. The effects of GTS-21 on these pro-/anti-inflammatory signaling molecules were reversed by treatment with an α7 nAChR antagonist, suggesting that the anti-inflammatory effects of GTS-21 are mediated through α7 nAChR activation. The anti-inflammatory and neuroprotective properties of GTS-21 were then confirmed in LPS-induced systemic inflammation and MPTP-induced PD model mice. In LPS-injected mouse brains, GTS-21 reduced microglial activation and production of proinflammatory markers. Furthermore, in the brains of MPTP-injected mice, GTS-21 restored locomotor activity and dopaminergic neuronal cell death while inhibiting microglial activation and pro-inflammatory gene expression. These findings suggest that GTS-21 has therapeutic potential in neuroinflammatory and neurodegenerative diseases such as PD. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.*
dc.languageEnglish*
dc.publisherMDPI*
dc.subjectGTS-21*
dc.subjectmicroglia*
dc.subjectmolecular mechanism*
dc.subjectneuroinflammation*
dc.subjectParkinson’s disease*
dc.subjectα7 nAChR agonist*
dc.titleAnti-Inflammatory and Neuroprotective Mechanisms of GTS-21, an α7 Nicotinic Acetylcholine Receptor Agonist, in Neuroinflammation and Parkinson’s Disease Mouse Models*
dc.typeArticle*
dc.relation.issue8*
dc.relation.volume23*
dc.relation.indexSCIE*
dc.relation.indexSCOPUS*
dc.relation.journaltitleInternational Journal of Molecular Sciences*
dc.identifier.doi10.3390/ijms23084420*
dc.identifier.wosidWOS:000785238400001*
dc.identifier.scopusid2-s2.0-85128502328*
dc.author.googlePark J.-E.*
dc.author.googleLeem Y.-H.*
dc.author.googlePark J.-S.*
dc.author.googleKim D.-Y.*
dc.author.googleKang J.L.*
dc.author.googleKim H.-S.*
dc.contributor.scopusid이지희(7404517577)-
dc.contributor.scopusid김희선(57191372551)-
dc.contributor.scopusid박진선(54914743600)-
dc.contributor.scopusid임예현(25422269100)-
dc.date.modifydate20220902081005*
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의과대학 > 의학과 > Journal papers
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