Urotensin-II Prevents Cartilage Degeneration in a Monosodium Iodoacetate-Induced Rat Model of Osteoarthritis

Terzi̇, Menderes Yusuf; Okuyan, Hamza Malik; Karaboğa, İhsan; Gökdemir, Cemil Emre; Tap, Duygu; Kalacı, Aydıner

doi:10.1007/s10989-022-10448-4

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“…Joint samples were handled and processed for histological examinations as described previously. [ 17 ] Briefly, the dissected tissues were fixed at room temperature with 10% neutral buffered formalin for three days and were kept for demineralization in 10% formic acid solution for 12 h after the fixation stage. Afterward, dehydration was performed with ascending percentage of ethanol and absolute xylene.…”

Section: Methodsmentioning

confidence: 99%

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

Emre Gökdemir,

Malik Okuyan,

Karaboğa

et al. 2024

Arch Rheumatol

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Objectives: 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-κB) 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-κB 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-κB levels. Further experimental research would make significant contributions to a better understanding of the therapeutic effect of UCMA on degenerative cartilage tissues.

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Section: Methodsmentioning

confidence: 99%