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Öğe Ebselen, an Active Seleno-Organic Compound, Alleviates Articular Cartilage Degeneration in a Rat Model of Knee Osteoarthritis(Springernature, 2022) Okuyan, Hamza Malik; Yurtal, Ziya; Karaboğa, İhsan; Kaçmaz, 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 Prenatal immobility stress: Relationship with oxidative stress, inflammation, apoptosis, and intrauterine growth restriction in rats(Wiley, 2023) Kaya, Sinem Albayrak; Okuyan, Hamza Malik; Erboga, Zeynep Fidanol; Guzel, Savas; Yilmaz, Ahsen; Karaboga, IhsanBackgroundPrenatal stress is a significant risk factor affecting pregnant women and fetal health. In the present study, we aimed to investigate the effect of immobility stress at different periods of pregnancy on oxidative stress, inflammation, placental apoptosis and intrauterine growth retardation in rats.MethodsFifty adult virgin female Wistar albino rats were used. Pregnant rats were exposed to 6 h/day immobilization stress in a wire cage at different stages of pregnancy. Groups I and II (Day 1-10 stress group) were sacrificed on the 10th day of pregnancy, and Group III, Group IV (10-19th-day stress group), and Group V (1-19th-day stress group) were sacrificed on the 19th day of pregnancy. Inflammatory cytokines, including interleukin-6 (IL-6) and interleukin-10 (IL-10), serum corticotropin-releasing hormone (CRH), and corticosterone levels were measured by enzyme-linked immunosorbent assay. Malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels in the placenta were spectrophotometrically measured. Histopathological analyses of the placenta were evaluated by hematoxylin and eosin staining. Tumor necrosis factor-alpha (TNF-a) and caspase-3 immunoreactivity in placenta tissues were determined by the indirect immunohistochemical method. Placental apoptosis was determined by the TUNEL staining method.ResultsWe found that the immobility stress during pregnancy significantly increased serum corticosterone levels. Our results showed that the immobility stress diminished the number and weight of fetuses in rats compared to the non-stress group. The immobility stress caused significant histopathological changes in the connection zone and labyrinth zone and increased placental TNF-a and caspase-3 immunoreactivity and placental apoptosis. In addition, immobility stress significantly increased the levels of pro-inflammatory IL-6 and MDA and caused a significant decrease in the levels of antioxidant enzymes such as SOD, CAT, and anti-inflammatory IL-10.ConclusionsOur data suggest that immobility stress causes intrauterine growth retardation by activating the hypothalamic-pituitary-adrenal axis and deteriorating placental histomorphology and deregulating inflammatory and oxidative processes.Öğe Urotensin-II Prevents Cartilage Degeneration in a Monosodium Iodoacetate-Induced Rat Model of Osteoarthritis(Springer, 2022) Terzi, Menderes Yusuf; Okuyan, Hamza Malik; Karaboğa, İhsan; Gökdemir, Cemil Emre; Tap, Duygu; Kalaci, AydinerOsteoarthritis (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; Kalaci, Aydiner[Abstract Not Available]
