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Copyright (c) 2024 Arif Osman Tokat, Osman ÖZTÜRK, Aslı OKAN, Sümeyye UÇAR, Ece EROĞLU, Züleyha DOĞANYİĞİT, Mert OCAK, Şükrü ATEŞ, Seher YILMAZ
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The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Investigation of the effects of melatonin on lung tissue through the NLRP3/TLR2/NEK7 pathway in an experimental endotoxemia model
Corresponding Author(s) : Arif Osman Tokat
Cellular and Molecular Biology,
Vol. 70 No. 10: Issue 10
Abstract
Sepsis, a severe clinical syndrome, arises from pro-inflammatory and apoptotic processes. Its rapid progression from sepsis to severe stages necessitates timely intervention. The lipopolysaccharide (LPS) agent triggers pro-inflammatory mediator release through Toll-like receptors, particularly TLR-2, a vital biomarker in sepsis with multiple organ failure. In LPS-induced septic shock, the NEK7-mediated NLRP3 inflammasome pathway, linked to acute lung injury, is suppressed. This pathway is implicated in sepsis-induced platelet activation and septic shock development. Antioxidants like melatonin (MEL) may positively impact reducing septic shock. In microbial-induced sepsis, melatonin can regulate pro-inflammatory mediator transcriptional activation, potentially controlling the pro-inflammatory state. In the project, the histopathological impact of melatonin in lung tissue during endotoxic shock induced by the LPS agent in Sprague-Dawley rats, and its immunoreactivity to NLRP3/NEK7/TLR-2 molecules, were assessed. Lung volumes were evaluated using micro-computed tomography (Micro-CT). While bleeding, cell infiltration, and thickening of the alveolar wall were observed in the lungs of the LPS group, a reduction in these symptoms was noted in the MEL+LPS group. Expressions of NEK7, TLR2, and NLRP3 increased in both the LPS and MEL+LPS groups compared to the control group. It was determined that in the MEL+LPS group, levels of NEK7, TLR2, and Malondialdehyde (MDA) decreased compared to the LPS group. Additionally, a decrease in the total volume of lung tissue was observed in the LPS group. In this context, our study reported the therapeutic effect of melatonin on sepsis-related acute lung injury. Our study suggests that melatonin administration in the experimental endotoxemia model melatonin may help reduce lung damage by inhibiting NEK7 and TLR2 expressions.
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