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Öğe Comparison of the protective effect of the upper zone of the growth plate and unique cartilage matrix-associated protein with hyaluronic acid and corticosteroids on an experimental rat osteoarthritis model(Turkish League Against Rheumatism, 2024) Gokdemir, Cemil Emre; Okuyan, Hamza Malik; Karaboga, Ihsan; Terzi, Menderes Yusuf; Kalacı, AydınerObjectives: This study sought to compare the protective effect of the upper zone of the growth plate and unique cartilage matrix-associated protein (UCMA) with hyaluronic acid (HA) and corticosteroids (CS) in a rat model of osteoarthritis (OA). Materials and methods: In the experimental animal study, 40 adult male rats were randomly assigned into five groups: control, monosodium iodoacetate (MIA) + vehicle (MIA+V), MIA+HA, MIA+CS, and MIA+UCMA. The OA model was induced by an intra-articular MIA injection to the right knee, and intra-articular injections into the right knee were performed on the treatment groups seven times every three days for 21 days. The knee joints were taken for histopathology and immunohistochemistry (IHC) analyses after the rats were sacrificed. All sections were stained with hematoxylin-eosin, safranin O and fast green FCF, and toluidine blue, and bone morphogenetic protein 2 (BMP-2) and nuclear factor-kappa B (NF-kappa B) expressions were analyzed with IHC. The Mankin scoring was utilized to determine the histopathological changes in the joint tissues. Results: Mankin score was significantly higher in the MIA group compared to the control group. Histopathologically, in the UCMA-, HA-, and CS-treated groups, degenerations in the articular cartilage were milder than in the MIA+V group. Mankin score was found to be decreased significantly in the UCMA-, HA-, and CS-treated groups compared to the MIA group. Furthermore, IHC analyses revealed that NF-kappa B and BMP-2 expressions elevated in the MIA-induced OA model, while they were downregulated after UCMA, HA, and CS treatments. Conclusion: Our data revealed that UCMA could be used as a potential protective molecule in the prevention and treatment of OA. Furthermore, the protective effect of UCMA was similar to HA and CS, and its possible beneficial roles against OA may be linked to the reduced BMP-2 and NF-kappa B levels. Further experimental research would make significant contributions to a better understanding of the therapeutic effect of UCMA on degenerative cartilage tissues.Öğe Ebselen, an Active Seleno-Organic Compound, Alleviates Articular Cartilage Degeneration in a Rat Model of Knee Osteoarthritis(Springernature, 2023) Okuyan, Hamza Malik; Yurtal, Ziya; Karaboga, Ihsan; Kacmaz, Filiz; Kalacı, AydınerOsteoarthritis (OA) is a prevalent articular disease mainly characterized by extracellular matrix degradation, apoptosis, and inflammation, which lead to cartilage destruction and abnormal bone metabolism. With undesirable side effects, current limited symptomatic treatments are aimed at relieving pain and improving joint mobility in patients with OA. Intra-articular (IA) hyaluronic acid (HA) injection, as a nonsurgical therapy, is commonly used in the clinical management of knee OA, but the efficacy of this therapeutic option remains controversial. Ebselen has tremendous pharmacological importance for some diseases due to its antioxidant, antiapoptotic, and anti-inflammatory features. However, there is no research examining the therapeutic effect of Ebselen in OA using the rat OA model. Therefore, we aimed to investigate the therapeutic effect of Ebselen on cartilage degeneration and its role in bone morphogenetic protein 2 (BMP2) and nuclear factor kappa B (NF-kappa B) signaling in the molecular pathogenesis of OA. We induced a knee OA model in rats with an IA injection of monosodiumiodoacetate (MIA). After the treatment of Ebselen, we evaluated its chondroprotective effects by morphological, histopathological, and immunohistochemical methods and an enzyme-linked immunosorbent assay. We report for the first time that Ebselen treatment alleviated articular cartilage degeneration in the rat knee OA model and reduced MIA-induced BMP2 and NF-kappa B expressions. In addition, our results unveiled that Ebselen decreased IL-beta and IL-6 levels but did not affect COMP levels in the rat serum. Ebselen could be a promising therapeutic drug for the prevention and treatment of OA by alleviating cartilage degeneration and regulating BMP2 and NF-kappa B expressions.Öğe In vivo protective effects of upper zone of growth plate and cartilage matrix associated protein against cartilage degeneration in a monosodium iodoacetate induced osteoarthritis model(Canadian Science Publishing, 2020) Okuyan, Hamza Malik; Terzi, Menderes Yusuf; Karaboga, Ihsan; Dogan, Serdar; Kalacı, AydınerOsteoarthritis (OA) is a degenerative disease affecting the majority of over 65 year old people and characterized by cartilage degeneration, subchondral abnormal changes, and inflammation. Despite the enormous socioeconomic burden caused by OA, currently, there is no effective therapy against it. Upper zone of growth plate and cartilage matrix associated protein (UCMA) is a vitamin K dependent protein and has a critical role in pathophysiological conditions associated with bone and cartilage. However, there is no research on the protective role of intra-articular UCMA treatment in OA pathogenesis. Therefore, we aimed to investigate the potential therapeutic role of UCMA in an in vivo model of OA. We report for the first time that intra-articular UCMA injection ameliorated cartilage degeneration in a monosodium iodoacetate induced OA rat model. Furthermore, the OA-induced activation of nuclear factor kappa B and bone morphogenetic protein 2 signals was attenuated by UCMA. Our results indicated that UCMA decreased cartilage oligomeric matrix protein levels but did not affect interleukin 6, total antioxidant status, and total oxidant status levels in the serum. In conclusion, UCMA exhibited a therapeutic potential in the treatment of OA. This protective effect of UCMA is possibly achieved by reducing the aggrecanase activity and the production of inflammatory cytokines.Öğe Urotensin-II Prevents Cartilage Degeneration in a Monosodium Iodoacetate-Induced Rat Model of Osteoarthritis(Springer, 2022) Terzi, Menderes Yusuf; Okuyan, Hamza Malik; Karaboga, Ihsan; Gokdemir, Cemil Emre; Tap, Duygu; Kalacı, AydınerOsteoarthritis (OA) is a common degenerative articular disorder caused by traumatic or spontaneous factors such as genetics, obesity, and advanced age. Comprehending the pathogenic mechanism of OA ensures the development of novel disease-modifying therapeutics rather than conventional palliative drugs with undesired side effects. Urotensin-II (UII) is a multifunctional short cyclic peptide implicated in several disorders. We aimed to analyze the effects of intraarticular UII treatment in a monosodium iodoacetate (MIA)-induced OA rat model. We divided animals into six groups to test three different concentrations of UII with histopathological and immunohistochemical analyses of bone morphogenetic protein-2 (BMP-2), nuclear factor kappa B subunit 1 (NF-kappa B), and intrinsic UII expression. We analyzed serum levels of cartilage related and inflammatory markers post-OA. We observed a noticeable amelioration of the MIA-induced knee damage in UII-treated animals after gross morphology examination. Mankin scoring after histopathological stainings revealed a partial prevention of articular tissue damage in UII-treated animals. We found a significant reduction in BMP-2 and NF-kappa B while an increase in intrinsic UII expressions upon exogenous UII injection after immunohistochemical analyses. The Mankin scores were significantly correlated with BMP-2, NF-kappa B, and intrinsic UII levels. There was no significant alteration in serum markers after UII treatment. We are the first group showing the protective effect of UII on the destructed knee joints of osteoarthritic rats by downregulating the BMP-2 and NF-kappa B and upregulating intrinsic UII expressions. To uncover the mechanistic role of UII during OA, further experiments are warranted. [GRAPHICS] .Öğe Urotensin-II Prevents Cartilage Degeneration in a Monosodium Iodoacetate-Induced Rat Model of Osteoarthritis (vol 28, 140, 2022)(Springer, 2024) Terzi, Menderes Yusuf; Okuyan, Hamza Malik; Karaboga, Ihsan; Gokdemir, Cemil Emre; Tap, Duygu; Kalacı, Aydıner[Abstract Not Available]
