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?

Basit Öğe Kaydı
dc.authoridOzbek, hanefi/0000-0002-8084-7855
dc.authoridYILMAZ, Ibrahim/0000-0003-2003-6337
dc.authorwosidOzbek, hanefi/O-3472-2019
dc.contributor.authorYilmaz, I
dc.contributor.authorAkalan, H.
dc.contributor.authorOznam, K.
dc.contributor.authorKaraarslan, N.
dc.contributor.authorSirin, D. Yasar
dc.contributor.authorOzbek, H.
dc.date.accessioned2023-03-22T19:47:25Z
dc.date.available2023-03-22T19:47:25Z
dc.date.issued2022
dc.departmentBelirleneceken_US
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.en_US
dc.identifier.endpage4827en_US
dc.identifier.issn1128-3602
dc.identifier.issue13en_US
dc.identifier.pmid35856374en_US
dc.identifier.scopus2-s2.0-85134249183en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage4816en_US
dc.identifier.urihttps://hdl.handle.net/20.500.14034/691
dc.identifier.volume26en_US
dc.identifier.wosWOS:000837256500034en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherVerduci Publisheren_US
dc.relation.journalEuropean Review For Medical And Pharmacological Sciencesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectDegenerationen_US
dc.subjectInflammationen_US
dc.subjectNF-kappa Ben_US
dc.subjectNLRP3 inflammasomeen_US
dc.subjectOseltamiviren_US
dc.subjectIntervertebral Disc Degenerationen_US
dc.subjectHif-1-Alpha/Vegf Pathwayen_US
dc.subjectHippocampal Tissueen_US
dc.subjectInfluenzaen_US
dc.subjectRaten_US
dc.subjectIl-1-Betaen_US
dc.subjectCartilageen_US
dc.subjectTherapyen_US
dc.subjectHypoxiaen_US
dc.subjectVirusen_US
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?en_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayınlar Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu