Can transcription factors in the intervertebral disc of lopinavir/ritonavir prevent degeneration in the nucleus pulposus by mediating the regulation of inflammation through signaling pathways?

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dc.authoridOzbek, hanefi/0000-0002-8084-7855
dc.authorwosidOzbek, hanefi/O-3472-2019
dc.contributor.authorYılmaz, I.
dc.contributor.authorAkalan, Hande
dc.contributor.authorKaraarslan, N.
dc.contributor.authorŞirin, Duygu Yaşar
dc.contributor.authorKaplan, N.
dc.contributor.authorDoğan, Mustafa
dc.contributor.authorÖzbek, H.
dc.date.accessioned2023-05-06T17:18:25Z
dc.date.available2023-05-06T17:18:25Z
dc.date.issued2022
dc.departmentFakülteler, Fen Edebiyat Fakültesi, Biyoloji Bölümü
dc.departmentYüksekokullar, Sağlık Yüksekokulu, Beslenme ve Diyetetik Bölümü
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Enfeksiyon Hastalıkları Ana Bilim Dalı
dc.description.abstractOBJECTIVE: This study was con-ducted to examine whether lopinavir/ritonavir (Lop/r), an HIV protease inhibitor, can improve disc physiology and slow down intervertebral disc (IVD) degeneration through in vitro experimental methods, as well as whether it can suppress inflammation with interleukin-1 beta (IL-113) and sex-determining region Y (SRY) protein-related high-mobility group box genes-9 (SOX9) through hypoxia-inducible factor 1-alpha (HIF-1 alpha) and the nuclear factor kappa B (NF-KB) signaling pathway. The aim was to investigate whether Lop/r application is toxic to IVD cells and the microenvironment simultaneously. PATIENTS AND METHODS: Human primary cell cultures were prepared using herniated IVD tissues obtained from patients with lumbar disc hernia who were unresponsive to conservative and medical treatment, and thereby, were operated on. The untreated culture samples served as control group, and the samples treated with Lop/r served as study group. Microscopic evaluations were performed simultaneously using fluorescent and supravital dyes in all groups. In addition to cell viability, toxicity, and proliferation analysis through a commercial kit, IL-113, SOX9, HIF-1 alpha, and NF-KB protein expressions were evaluated using Western blotting. In the statistical comparison of the obtained data, an alpha value less than 0.05 was considered significant. RESULTS: Cell proliferation decreased in the Lop/r group, but no cell death was observed (p < 0.05). Moreover, at the end of 72 hours after Lop/r application, IL-113 and NF-kB protein expressions decreased by 40% and 52%, respectively, while HIF-1 alpha and SOX9 protein expressions increased by 4% and 59%, respectively (p < 0.05). CONCLUSIONS: Although these data were obtained from an in vitro experimental study, it is believed that these findings could make significant contributions to the pharmaco-regenerative treatment modalities of IVD degeneration. Lop/r suppresses the IL-113 and NF-KB and induces SOX9 and HIF-1 alpha, since these signaling path-ways may be related to human IVD degeneration.
dc.identifier.endpage6855
dc.identifier.issn1128-3602
dc.identifier.issue18en_US
dc.identifier.pmid36196733
dc.identifier.startpage6845
dc.identifier.urihttps://hdl.handle.net/20.500.11776/11816
dc.identifier.volume26
dc.identifier.wosWOS:000876873600014
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakPubMed
dc.institutionauthorAkalan, Hande
dc.institutionauthorŞirin, Duygu Yaşar
dc.institutionauthorDoğan, Mustafa
dc.language.isoen
dc.publisherVerduci Publisher
dc.relation.ispartofEuropean Review For Medical And Pharmacological Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAutophagy
dc.subjectDisc degeneration
dc.subjectHypoxia
dc.subjectInflamma-tion
dc.subjectLop/r
dc.subjectSOX9
dc.subjectNf-Kappa-B
dc.subjectCells
dc.subjectPharmacokinetics
dc.subjectInhibitors
dc.subjectIl-1-Beta
dc.subjectApoptosis
dc.subjectTissue
dc.titleCan transcription factors in the intervertebral disc of lopinavir/ritonavir prevent degeneration in the nucleus pulposus by mediating the regulation of inflammation through signaling pathways?
dc.typeArticle

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