Does nimodipine, a selective calcium channel blocker, impair chondrocyte proliferation or damage extracellular matrix structures?

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dc.authorid0000-0002-8084-7855en_US
dc.authorid0000-0003-2003-6337en_US
dc.authorid0000-0002-5412-8355
dc.contributor.authorKaplan, Necati
dc.contributor.authorYılmaz, İbrahim
dc.contributor.authorKaraarslan, Numan
dc.contributor.authorKaya, Yasin Emre
dc.contributor.authorŞirin, Duygu Y.
dc.contributor.authorÖzbek, Hanefi
dc.date.accessioned2021-06-23T19:52:21Z
dc.date.available2021-06-23T19:52:21Z
dc.date.issued2019
dc.departmentBAİBÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümüen_US
dc.description.abstractBackground: The study aimed to investigate the effects of the active ingredient, nimodipine, on chondrocyte proliferation and extracellular matrix (ECM) structures in cartilage tissue cells. Methods: Chondrocyte cultures were prepared from tissues resected via surgical operations. Nimodipine was then applied to these cultures and molecular analysis was performed. The data obtained were statistically calculated. Results: Both, the results of the (3-(4,5 dimethylthiazol2-yl)-2,5-diphenyltetrazolium (MTT) assay and the fluorescence microscope analysis [a membrane permeability test carried out with acridine orange/propidium iodide staining (AO/PI)] confirmed that the active ingredient, nimodipine, negatively affects the cell cultures. Conclusion: Nimodipine was reported to suppress cellular proliferation; chondroadherin (CHAD) and hypoxia-inducible factor-1 alpha (HIF-1 alpha) expression thus decreased by 2.4 and 1.7 times, respectively, at 24 hrs when compared to the control group (p < 0.05). Furthermore, type II collagen (COL2A1) expression was not detected (p < 0.05). The risk that a drug prescribed by a clinician in an innocuous manner to treat a patient by relieving the symptoms of a disease may affect the proliferation, differentiation, and viability of other cells and/or tissues at the molecular level, beyond its known side effects or adverse events, should not be forgotten.en_US
dc.identifier.doi10.2174/1389201020666190506124548
dc.identifier.endpage524en_US
dc.identifier.issn1389-2010
dc.identifier.issn1873-4316
dc.identifier.issue6en_US
dc.identifier.pmid31057106en_US
dc.identifier.startpage517en_US
dc.identifier.urihttps://doi.org/10.2174/1389201020666190506124548
dc.identifier.urihttps://hdl.handle.net/20.500.12491/10136
dc.identifier.volume20en_US
dc.identifier.wosWOS:000576827500002en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorKaya, Yasin Emre
dc.language.isoenen_US
dc.publisherBentham Science Publ Ltden_US
dc.relation.ispartofCurrent Pharmaceutical Biotechnologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectChondroadherinen_US
dc.subjectChondrocyteen_US
dc.subjectHypoxia-inducible factor-1 Alphaen_US
dc.subjectNimodipineen_US
dc.subjectType II Collagenen_US
dc.subjectMatrix Structuresen_US
dc.titleDoes nimodipine, a selective calcium channel blocker, impair chondrocyte proliferation or damage extracellular matrix structures?en_US
dc.typeArticleen_US

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