The melatonin agonist ramelteon attenuates bleomycin-induced lung fibrosis by suppressing the NLRP3/TGF-?1/HMGB1 signaling pathway

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dc.contributor.authorAydin, Pelin
dc.contributor.authorAksakalli-Magden, Zeynep B.
dc.contributor.authorCivelek, Maide S.
dc.contributor.authorKarabulut-Uzuncakmak, Sevgi
dc.contributor.authorMokhtare, Behzad
dc.contributor.authorOzkaraca, Mustafa
dc.contributor.authorAlper, Fatih
dc.date.accessioned2024-10-26T18:08:07Z
dc.date.available2024-10-26T18:08:07Z
dc.date.issued2023
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractPurpose: The possible effects of ramelteon, a melatonin receptor agonist on bleomycin-induced lung fibrosis were analyzed via transforming growth factor beta 1 (TGF-beta 1), the high mobility group box 1 (HMGB1) and Nod-like receptor pyrin domain-containing 3 (NLRP3) which are related to the fibrosis process. Materials and methods: Bleomycin (0.1 mL of 5 mg/kg) was administered by intratracheal instillation to induce pulmonary fibrosis (PF). Starting 24 h after bleomycin administration, a single dose of ramelteon was administered by oral gavage to the healthy groups, i.e. PF + RM2 (pulmonary fibrosis model with bleomycin + ramelteon at 2 mg/kg) and PF + RM4 (pulmonary fibrosis model with bleomycin + ramelteon at 4 mg/kg) at 2 and 4 mg/kg doses, respectively. Real-time polymerase chain reaction (real-time PCR) analyses, histopathological, and immunohistochemical staining were performed on lung tissues. Lung tomography images of the rats were also examined. Results: The levels of TGF-beta 1, HMGB1, NLRP3, and interleukin 1 beta (IL-1 beta) mRNA expressions increased as a result of PF and subsequently decreased with both ramelteon doses (p < 0.0001). Both doses of ramelteon partially ameliorated the reduction in the peribronchovascular thickening, ground-glass appearances, and reticulations, and the loss of lung volume. Conclusions: The severity of fibrosis decreased with ramelteon application. These effects of ramelteon may be associated with NLRP3 inflammation cascade.
dc.identifier.doi10.1016/j.advms.2023.09.004
dc.identifier.endpage331
dc.identifier.issn1896-1126
dc.identifier.issn1898-4002
dc.identifier.issue2
dc.identifier.pmid37716182
dc.identifier.scopus2-s2.0-85170695078
dc.identifier.scopusqualityQ2
dc.identifier.startpage322
dc.identifier.urihttps://doi.org/10.1016/j.advms.2023.09.004
dc.identifier.urihttps://hdl.handle.net/20.500.12418/29813
dc.identifier.volume68
dc.identifier.wosWOS:001165138800001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Urban & Partner Sp Z O O
dc.relation.ispartofAdvances in Medical Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectMelatonin
dc.subjectRamelteon
dc.subjectFibrosis
dc.subjectNLRP3
dc.subjectTGF-beta 1
dc.titleThe melatonin agonist ramelteon attenuates bleomycin-induced lung fibrosis by suppressing the NLRP3/TGF-?1/HMGB1 signaling pathway
dc.typeArticle

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