<?xml version="1.0" encoding="UTF-8"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-10-29T22:39:25Z</responseDate><request verb="GetRecord" identifier="oai:bayburt-rdlopen.rawdatalibrary.net:bayburt/11882" metadataPrefix="oai_dc">https://bayburt-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:bayburt-rdlopen.rawdatalibrary.net:bayburt/11882</identifier><datestamp>2026-10-29T19:41:58Z</datestamp><setSpec>openaire</setSpec><setSpec>com_bayburt_10000</setSpec><setSpec>col_bayburt_10001</setSpec><setSpec>com_bayburt_10010</setSpec><setSpec>col_bayburt_10222</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:title>The melatonin agonist ramelteon attenuates bleomycin-induced lung fibrosis by suppressing the NLRP3/TGF-Β1/HMGB1 signaling pathway</dc:title><dc:creator>Aydin, Pelin</dc:creator><dc:creator>Aksakalli-Magden, Zeynep B.</dc:creator><dc:creator>Civelek, Maide S.</dc:creator><dc:creator>Karabulut-Uzuncakmak, Sevgi</dc:creator><dc:creator>Mokhtare, Behzad</dc:creator><dc:creator>Ozkaraca, Mustafa</dc:creator><dc:creator>Alper, Fatih</dc:creator><dc:creator>Halici, Zekai</dc:creator><dc:subject>Fibrosis</dc:subject><dc:subject>Melatonin</dc:subject><dc:subject>NLRP3</dc:subject><dc:subject>Ramelteon</dc:subject><dc:subject>TGF-β1</dc:subject><dc:description>Purpose: The possible effects of ramelteon, a melatonin receptor agonist on bleomycin-induced lung fibrosis were analyzed via transforming growth factor β1 (TGF-β1), 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-β1, HMGB1, NLRP3, and interleukin 1 beta (IL-1β) mRNA expressions increased as a result of PF and subsequently decreased with both ramelteon doses (p ​&lt; ​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:description><dc:publisher>Medical University of Bialystok</dc:publisher><dc:date>2023</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/bayburt/11882</dc:identifier><dc:identifier>https://doi.org/10.1016/j.advms.2023.09.004</dc:identifier><dc:identifier>1896-1126</dc:identifier><dc:language>en</dc:language><dc:relation>Advances in Medical Sciences</dc:relation><dc:rights>info:eu-repo/semantics/closedAccess</dc:rights><dc:type>info:eu-repo/semantics/article</dc:type><dc:identifier>https://bayburt-rdlopen.rawdatalibrary.net/tr/items/bayburt/11882</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>