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자료유형
학술저널
저자정보
강진석 (남서울대학교)
저널정보
충북대학교 동물의학연구소 Journal of Biomedical and Translational Research Journal of Biomedical and Translational Research 제19권 제3호
발행연도
2018.9
수록면
43 - 48 (6page)

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This study was carried out to investigate the protectiveeffect of prednisolone in rabbitprimary cultured articular chondrocytes treated with sodiumnitroprusside (SNP), a nitric oxide donor. After cell phenotype was determined, the MTT assay and Western blot analysis of type II collagen, cylooxygenase-2 (COX-2) and phosphorylatedextracellular regulated kinase (pERK) were performed in control, SNP(298μg/ml) alone orSNP plus prednisolone (0.05-50 μg/ml)-treated rabbit articular chondrocytes. Immunofluorescence staining of type II collagen was also performed. Cell morphology indicated that SNP treatment induced cytotoxicity, and that SNP-induced cytotoxicity was inhibited by prednisolone treatment. MTT assay showed thatSNP treatment decreasedsignificantly the level of cell viability comparedwith that of control (p<0.01), and that prednisolonetreatment decreased SNP-induced cytotoxicity.SNPtreatment decreased type II collagen compared with control chondrocytes, and prednisolone treatment recovered the down-regulatedexpression of type IIcollagen inducedby SNP, showing a significant level in 5 μg/ml of the prednisolone treatment group compared to the SNPtreatment group (p < 0.05). Increase of COX-2 was significantly induced by SNP treatment compared to control chondrocytes (p<0.01), and COX-2 expression was decreased by prednisolone treatment, showing a significant level in 50 μg/ml of theprednisolone treatment group compared to theSNP treatment group (p < 0.05). Immunofluorescence staining confirmed these phenomena. Furthermore, SNP treatment significantly induced a decrease of pERK expression compared tocontrol chondrocytes (p<0.01), and prednisolonetreatment recovered its expression, showing a significant level in 0.5 μg/ml of the prednisolone treatment group compared to the SNPtreatment group (p < 0.05). Taken together, prednisolone inhibited SNP-induced celldeath and dedifferentiation, and modulated expression of COX-2 and pERK inrabbit articular chondrocytes.

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