Does oseltamivir protect human chondrocyte and nucleus pulposus cells from degeneration by inhibiting senescence and proinflammation mediated by the NLRP3 inflammasome and NF-kappa B?

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dc.authoridYILMAZ, Ibrahim/0000-0003-2003-6337
dc.authorscopusid35197435300
dc.authorscopusid57216912962
dc.authorscopusid56891784100
dc.authorscopusid56674583800
dc.authorscopusid56769801000
dc.authorscopusid7005912992
dc.contributor.authorYılmaz, İbrahim
dc.contributor.authorAkalan, Hande
dc.contributor.authorÖznam, K.
dc.contributor.authorKaraarslan, Numan
dc.contributor.authorŞirin, Duygu Yaşar
dc.contributor.authorÖzbek, Hanefi
dc.date.accessioned2023-04-20T08:01:11Z
dc.date.available2023-04-20T08:01:11Z
dc.date.issued2022
dc.departmentFakülteler, Fen Edebiyat Fakültesi, Biyoloji Bölümü
dc.departmentYüksekokullar, Sağlık Yüksekokulu, Beslenme ve Diyetetik Bölümü
dc.description.abstractOBJECTIVE: Recent drug design studies suggest that inflammation is among the most important factors in the development of both intervertebral disc (IVD) degeneration (IVDD) and osteoarthritis (OA) due to cartilage damage. This study aimed to investigate whether the anti-inflammatory drug oseltamivir has a toxic effect on IVD and cartilage tissue cells. It assessed what effect oseltamivir has on hypoxia-inducible factor (HIF)-1 alpha (HIF1 alpha), which plays an important role in anabolic pathways in IVD and cartilage tissue. In addition, the study analyzed whether oseltamivir could inhibit the release of inflammatory interleukin-1 beta (IL-1 beta) via the nuclear factor kappa-B (NF-kappa B) signaling pathway by activating the nucleotide-binding oligomerization domain and leucine-rich repeat protein-3 (NLRP3) inflammasome. MATERIALS AND METHODS: Human lumbar IVD (n = 8) tissues were isolated for annulus fibrosus (AF) and nucleus pulposus (NP) primary cell cultures. and human tibial and femoral cartilage tissues (n = 8) were isolated for primary chondrocyte cultures. Untreated groups served as the control and oseltamivir-treated groups as the study sample. Cell viability and cytotoxicity were evaluated at 0, 24, 48. and 72 h in all groups for changes in HIF-1 alpha, IL-18, NF-kappa B. and the NLRP3-inflammasome protein expressions using Western blotting. The a significance value was < 0.05. RESULTS: In the oseltamivir-treated groups, cell proliferation decreased in both AF/NP cell and chondrocyte cultures obtained from IVD cartilage tissues. After Western blotting analysis, changes were observed in the protein expressions of HIF-1 alpha, IL-1 beta, NF-kappa B, and the NLRP3 inflammasome in both AF/NP cells and chondrocytes. The results were statistically significant (p < 0.05). CONCLUSIONS: Oseltamivir treatment may be a promising regenerative strategy to manage IVDD and osteoarthritic cartilage tissues.
dc.identifier.doi10.26355/eurrev_202207_29207
dc.identifier.endpage4827
dc.identifier.issn1128-3602
dc.identifier.issue13en_US
dc.identifier.pmid35856374
dc.identifier.scopus2-s2.0-85134249183
dc.identifier.scopusqualityQ2
dc.identifier.startpage4816
dc.identifier.urihttps://doi.org/10.26355/eurrev_202207_29207
dc.identifier.urihttps://hdl.handle.net/20.500.11776/10784
dc.identifier.volume26
dc.identifier.wosWOS:000837256500034
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorAkalan, Hande
dc.institutionauthorŞirin, Duygu Yaşar
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.subjectDegeneration
dc.subjectInflammation
dc.subjectNf-Kappa B
dc.subjectNlrp3 Inflammasome
dc.subjectOseltamivir
dc.subjectIntervertebral Disc Degeneration
dc.subjectHif-1-Alpha/Vegf Pathway
dc.subjectHippocampal Tissue
dc.subjectInfluenza
dc.subjectRat
dc.subjectIl-1-Beta
dc.subjectCartilage
dc.subjectTherapy
dc.subjectHypoxia
dc.subjectVirus
dc.titleDoes oseltamivir protect human chondrocyte and nucleus pulposus cells from degeneration by inhibiting senescence and proinflammation mediated by the NLRP3 inflammasome and NF-kappa B?
dc.typeArticle

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