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The potential role of amlodipine on experimentally induced bacterial rhinosinusitis

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dc.contributor.author Tatar, Arzu
dc.contributor.author Korkmaz, Mukadder
dc.contributor.author Yayla, Muhammed
dc.contributor.author Polat, Elif
dc.contributor.author Uslu, Hakan
dc.contributor.author Halici, Zekai
dc.contributor.author Parlak, Secil N.
dc.date.accessioned 2024-03-19T06:57:28Z
dc.date.available 2024-03-19T06:57:28Z
dc.date.issued 2017
dc.identifier.citation Tatar, A., Korkmaz, M., Yayla, M., Polat, E., Uslu, H., Halici, Z., Parlak, SN. (2017). The potential role of amlodipine on experimentally induced bacterial rhinosinusitis. Braz. J. Otorhinolaryngol., 83(6), 619-626. https://doi.org/10.1016/j.bjorl.2016.08.006 en_US
dc.identifier.issn 1808-8694
dc.identifier.issn 1808-8686
dc.identifier.uri http://dx.doi.org/10.1016/j.bjorl.2016.08.006
dc.identifier.uri https://www.webofscience.com/wos/woscc/full-record/WOS:000417392200003
dc.identifier.uri http://earsiv.odu.edu.tr:8080/xmlui/handle/11489/4765
dc.description WoS Categories: Otorhinolaryngology en_US
dc.description Web of Science Index: Science Citation Index Expanded (SCI-EXPANDED) en_US
dc.description Research Areas: Otorhinolaryngology en_US
dc.description.abstract Introduction: Antibiotics are frequently used for the treatment of rhinosinusitis. Concerns have been raised regarding the adverse effects of antibiotics and growing resistance. The lack of development of new antibiotic compounds has increased the necessity for exploration of non-antibiotic compounds that have antibacterial activity. Amlodipine is a non-antibiotic compound with anti-inflammatory activity. Objective: In this study we aimed to investigate the potential role of amlodipine in the treatment of rhinosinusitis by evaluating its effects on tissue oxidative status, mucosal histology and inflammation. Methods: Fifteen adult albino guinea pigs were inoculated with Staphylococcus aureus and treated with saline, cefazolin sodium, or amlodipine for 7 days. The control group was composed by five healthy guinea pigs. Animals were sacrificed after the treatment. Histopathological changes were identified using Hematoxylin-Eosin staining. Inflammation was assessed by Polymorphonuclear Leukocyte infiltration density. Tissue levels of antioxidants (superoxide dismutase, glutathione) and an oxidative product (malondialdehyde) were determined. Results: In rhinosinusitis induced animals, amlodipine reduced loss of cilia, lamina propria edema and collagen deposition compared to placebo (saline) and although not superior to cefazolin, amlodipine decreased polymorphonuclear leukocyte infiltration. The superoxide dismutase activity and glutathione levels were reduced, whereas the malondialdehyde levels were increased significantly in all three-treatment groups compared to the control group. Amlodipine treated group showed significantly increased superoxide dismutase and glutathione levels and decreased malondialdehyde levels compared to all treatment groups. Conclusion: The non-antibiotic compound amlodipine may have a role in acute rhinosinusitis treatment through tissue protective, antioxidant and anti-inflammatory mechanisms. (C) 2016 Associacao Brasileira de Otorrinolaringologia e Cirurgia Cervico-Facial. Published by Elsevier Editora Ltda. en_US
dc.language.iso eng en_US
dc.publisher ASSOC BRASILEIRA OTORRINOLARINGOLOGIA & CIRURGIA CERVICOFACIAL-SAO PAULO en_US
dc.relation.isversionof 10.1016/j.bjorl.2016.08.006 en_US
dc.rights info:eu-repo/semantics/openAccess en_US
dc.subject Rhinosinusitis, Non-antibiotic, Amlodipine, Antioxidants, Guinea pig en_US
dc.subject IN-VITRO, ANTIBIOTICS, INFECTIONS, MANAGEMENT, TISSUE, INFLAMMASOME, ANTIOXIDANT, MECHANISMS, SINUSITIS, DAMAGE en_US
dc.title The potential role of amlodipine on experimentally induced bacterial rhinosinusitis en_US
dc.type article en_US
dc.relation.journal BRAZILIAN JOURNAL OF OTORHINOLARYNGOLOGY en_US
dc.contributor.department Ordu Üniversitesi en_US
dc.contributor.authorID 0000-0002-0659-3084 en_US
dc.contributor.authorID 0000-0001-6808-5467 en_US
dc.identifier.volume 83 en_US
dc.identifier.issue 6 en_US
dc.identifier.startpage 619 en_US
dc.identifier.endpage 626 en_US


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