Please use this identifier to cite or link to this item:
https://hdl.handle.net/20.500.11851/8372
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DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yıldırım, Sendegül | - |
dc.contributor.author | Özkan, Ayse | - |
dc.contributor.author | Aytaç, Güneş | - |
dc.contributor.author | Ağar, Aysel | - |
dc.contributor.author | Tanriover, Gamze | - |
dc.date.accessioned | 2022-01-15T13:02:41Z | - |
dc.date.available | 2022-01-15T13:02:41Z | - |
dc.date.issued | 2022 | - |
dc.identifier.issn | 0161-813X | - |
dc.identifier.issn | 1872-9711 | - |
dc.identifier.uri | https://doi.org/10.1016/j.neuro.2021.11.011 | - |
dc.identifier.uri | https://hdl.handle.net/20.500.11851/8372 | - |
dc.description.abstract | Neuroinflammation has an essential role in various neurodegenerative diseases including Parkinson's disease (PD). Microglial activation as a result of neuroinflammation exacerbates the pathological consequences of the disease. The toxic effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes alpha-synuclein (alpha-synuclein) accumulation, which leads to dopaminergic neuron death in the MPTP-induced mouse model. Toll-like receptor 4 (TLR4) stimulates release of cytokine through NF-kB by activating glial cells, thus resulting in the death of dopaminergic neurons. Melatonin has the ability to cross the blood-brain barrier and protect neurons through anti-inflammatory properties. We hypothesized that melatonin could suppress TLR4-mediated neuroinflammation, decrease cytokine release due to the inflammatory response, and reduce dopaminergic neuron loss in the MPTP-induced mouse model. In the MPTP-induced mouse model, we aimed to assess the neuroinflammatory responses caused by TLR4 activation as well as the effect of melatonin on these responses. Three-month-old male C57BL/6 mice were randomly divided into five groups; Control (Group-C), Sham (Group-S), Melatonin-treated (Group-M), MPTP-injected (Group-P), and MPTP + melatonin-injected (Group-P + M). MPTP toxin (20 mg/kg) was dissolved in saline and intraperitoneally (i.p.) injected to mice for two days with 12 h intervals. The total dose per mouse was 80 mg/kg. Melatonin was administered (20 mg/kg) intraperitoneally to Group-M and Group-P + M twice a day for five days. Eight days after starting the experiment, the motor activities of mice were evaluated by locomotor activity tests. The effects on dopamine neurons in the SNPc was determined by tyrosine hydroxylase (TH) immunohistochemistry. TLR4, alpha-synuclein, and p65 expression was evaluated by immunostaining as well. The amount of TNF-alpha in the total brain was evaluated by western blot analysis. In our results seen that locomotor activity was lower in Group-P compared to Group-C. However, melatonin administration was improved this impairment. MPTPcaused decrease in TH immuno-expression in dopaminergic neurons in Group-P. TLR4 (p < 0.001), alpha-synuclein (p < 0.001), and p65 (p < 0.01) immuno-expressions were also decreased in Group-P+M compared to Group-P (using MPTP). TNF-alpha expression was lower in Group-C, Group-S, Group-M, and Group-P+M, when compared to Group-P (p < 0.0001) due to the absence of inflammatory response. In conclusion, our study revealed that melatonin administration reduced alpha-synuclein aggregation and TLR4mediated inflammatory response in the MPTP-induced mouse model. | en_US |
dc.description.sponsorship | Akdeniz University Scientific Research ProjectsAkdeniz University [TYL-2018-3972] | en_US |
dc.description.sponsorship | This study was supported by Akdeniz University Scientific Research Projects with project number TYL-2018-3972 and a Master of Science thesis of Sendegul YILDIRIM. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Elsevier | en_US |
dc.relation.ispartof | Neurotoxicology | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | Parkinson's disease | en_US |
dc.subject | MPTP | en_US |
dc.subject | Dopaminergic neuron | en_US |
dc.subject | TLR4 | en_US |
dc.subject | Melatonin | en_US |
dc.subject | Alpha-Synuclein | en_US |
dc.subject | Oxidative Stress | en_US |
dc.subject | Nitric-Oxide | en_US |
dc.subject | Lewy Body | en_US |
dc.subject | L-Dopa | en_US |
dc.subject | Protects | en_US |
dc.subject | Neuroinflammation | en_US |
dc.subject | Dysfunction | en_US |
dc.subject | Mice | en_US |
dc.subject | Parkinsonism | en_US |
dc.title | Role of Melatonin in Tlr4-Mediated Inflammatory Pathway in the Mtpt-Induced Mouse Model | en_US |
dc.type | Article | en_US |
dc.department | Faculties, School of Medicine, Department of Basic Medical Sciences | en_US |
dc.department | Fakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü | tr_TR |
dc.identifier.volume | 88 | en_US |
dc.identifier.startpage | 168 | en_US |
dc.identifier.endpage | 177 | en_US |
dc.identifier.wos | WOS:000725646800003 | en_US |
dc.identifier.scopus | 2-s2.0-85119909985 | en_US |
dc.institutionauthor | Aytaç, Güneş | - |
dc.identifier.pmid | 34808223 | en_US |
dc.identifier.doi | 10.1016/j.neuro.2021.11.011 | - |
dc.authorscopusid | 57215874107 | - |
dc.authorscopusid | 57210236706 | - |
dc.authorscopusid | 57188768289 | - |
dc.authorscopusid | 35615592300 | - |
dc.authorscopusid | 6507986489 | - |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.identifier.scopusquality | Q2 | - |
item.openairetype | Article | - |
item.languageiso639-1 | en | - |
item.grantfulltext | none | - |
item.fulltext | No Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | 03.14. Department of Internal Medicine | - |
Appears in Collections: | PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection Temel Tıp Bilimleri Bölümü / Department of Basic Medical Sciences WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection |
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