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Deciphering the Potential Neuroprotective Effects of Luteolin against A beta(1)-(42)-Induced Alzheimer's Disease

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dc.contributor.authorAhmad, Sareer-
dc.contributor.authorJo, Myeung Hoon-
dc.contributor.authorIkram, Muhammad-
dc.contributor.authorKhan, Amjad-
dc.contributor.authorKim, Myeong Ok-
dc.date.accessioned2022-12-26T10:01:06Z-
dc.date.available2022-12-26T10:01:06Z-
dc.date.issued2021-09-
dc.identifier.issn1661-6596-
dc.identifier.issn1422-0067-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/3315-
dc.description.abstractThe current study was undertaken to unveil the protective effects of Luteolin, a natural flavonoid, against amyloid-beta (A beta(1)-(42))-induced neuroinflammation, amyloidogenesis, and synaptic dysfunction in mice. For the development of an AD mouse model, amyloid-beta (A beta(1)-(42), 5 mu L/5 min/mouse) oligomers were injected intracerebroventricularly (i.c.v.) into mice's brain by using a stereotaxic frame. After that, the mice were treated with Luteolin for two weeks at a dose of 80 mg/kg/day. To monitor the biochemical changes, we conducted western blotting and immunofluorescence analysis. According to our findings, the infusion of amyloid-beta activated c-Jun N-terminal kinases (p-JNK), p38 mitogen-activated protein kinases, glial fibrillary acidic protein (GFAP), and ionized calcium adaptor molecule 1 (Iba-1) in the cortex and hippocampus of the experimental mice; these changes were significantly inhibited in A beta(1)-(42) + Luteolin-treated mice. Likewise, we also checked the expression of inflammatory markers, such as p-nuclear factor-kB p65 (p-NF-kB p65 (Ser536), tissue necrosis factor (TNF-alpha), and Interleukin1-beta (IL-1 beta), in A beta(1)-(42)-injected mice brain, which was attenuated in A beta(1)-(42) + Luteolin-treated mice brains. Further, we investigated the expression of pro- and anti-apoptotic cell death markers such as Bax, Bcl-2, Caspase-3, and Cox-2, which was significantly reduced in A beta(1)-(42) + Lut-treated mice brains compared to the brains of the A beta-injected group. The results also indicated that with the administration of A beta(1)-(42), the expression levels of beta-site amyloid precursor protein cleaving enzyme (BACE-1) and amyloid-beta (A beta(1)-(42)) were significantly enhanced, while they were reduced in A beta(1)-(42) + Luteolin-treated mice. We also checked the expression of synaptic markers such as PSD-95 and SNAP-25, which was significantly enhanced in A beta(1)-(42) + Lut-treated mice. To unveil the underlying factors responsible for the protective effects of Luteolin against AD, we used a specific JNK inhibitor, which suggested that Luteolin reduced A beta-associated neuroinflammation and neurodegeneration via inhibition of JNK. Collectively, our results indicate that Luteolin could serve as a novel therapeutic agent against AD-like pathological changes in mice.-
dc.language영어-
dc.language.isoENG-
dc.publisherMDPI-
dc.titleDeciphering the Potential Neuroprotective Effects of Luteolin against A beta(1)-(42)-Induced Alzheimer's Disease-
dc.typeArticle-
dc.publisher.location스위스-
dc.identifier.doi10.3390/ijms22179583-
dc.identifier.scopusid2-s2.0-85114231253-
dc.identifier.wosid000694374500001-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.22, no.17-
dc.citation.titleINTERNATIONAL JOURNAL OF MOLECULAR SCIENCES-
dc.citation.volume22-
dc.citation.number17-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaChemistry-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryChemistry, Multidisciplinary-
dc.subject.keywordPlusAMYLOID-BETA PEPTIDE-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusKAPPA-B-
dc.subject.keywordPlusMICROGLIA-
dc.subject.keywordPlusNEUROINFLAMMATION-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusMODULATION-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusPATHOLOGY-
dc.subject.keywordPlusDYNAMICS-
dc.subject.keywordAuthoramyloid-beta-
dc.subject.keywordAuthorAlzheimer's disease-
dc.subject.keywordAuthorluteolin-
dc.subject.keywordAuthorneurodegeneration-
dc.subject.keywordAuthorneuroprotection-
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