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Lee WK, Kang JS. Modulation of Apoptosis and Differentiation by the Treatment of Sulfasalazine in Rabbit Articular Chondrocytes. Toxicol Res. 2016;32(2):115-21doi: 10.5487/TR.2016.32.2.115.
Lee, W. K., & Kang, J. S. (2016). Modulation of Apoptosis and Differentiation by the Treatment of Sulfasalazine in Rabbit Articular Chondrocytes. Toxicological research, 32(2), 115-21. https://doi.org/10.5487/TR.2016.32.2.115
Lee, Won Kil, and Kang, Jin Seok. "Modulation of Apoptosis and Differentiation by the Treatment of Sulfasalazine in Rabbit Articular Chondrocytes." Toxicological research vol. 32,2 (2016): 115-21. doi: https://doi.org/10.5487/TR.2016.32.2.115
Lee WK, Kang JS. Modulation of Apoptosis and Differentiation by the Treatment of Sulfasalazine in Rabbit Articular Chondrocytes. Toxicol Res. 2016 Apr;32(2):115-21. doi: 10.5487/TR.2016.32.2.115. Epub 2016 Apr 30. PMID: 27123162; PMCID: PMC4843981.
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Toxicol Res. 2016 Apr;32(2):115-21. doi: 10.5487/TR.2016.32.2.115. Epub 2016 Apr 30.

Modulation of Apoptosis and Differentiation by the Treatment of Sulfasalazine in Rabbit Articular Chondrocytes.

Toxicological research

Won Kil Lee, Jin Seok Kang

Affiliations

  1. Department of Biomedical Laboratory Science, Namseoul University, Cheonan, Korea.

PMID: 27123162 PMCID: PMC4843981 DOI: 10.5487/TR.2016.32.2.115

Abstract

This study was conducted to examine the cellular regulatory mechanisms of sulfasalazine (SSZ) in rabbit articular chondrocytes treated with sodium nitroprusside (SNP). Cell phenotype was determined, and the MTT assay, Western blot analysis and immunofluorescence staining of type II collagen was performed in control, SNP-treated and SNP plus SSZ (50~200 μg/mL) rabbit articular chondrocytes. Cellular proliferation was decreased significantly in the SNP-treated group compared with that in the control (p < 0.01). SSZ treatment clearly increased the SNP-reduced proliferation levels in a concentration-dependent manner (p < 0.01). SNP treatment induced significant dedifferentiation and inflammation compared with control chondrocytes (p < 0.01). Type II collagen expression levels increased in a concentration-dependent manner in response to SSZ treatment but were unaltered in SNP-treated chondrocytes (p < 0.05 and < 0.01, respectively). Cylooxygenase-2 (COX-2) expression increased in a concentration-dependent manner in response to SSZ treatment but was unaltered in SNP-treated chondrocytes (p < 0.05). Immunofluorescence staining showed that SSZ treatment increased type II collagen expression compared with that in SNP-treated chondrocytes. Furthermore, phosphorylated extracellular regulated kinase (pERK) expression levels were decreased significantly in the SNP-treated group compared with those in control chondrocytes (p < 0.01). Expression levels of pERK increased in a concentration-dependent manner by SSZ but were unaltered in SNP-treated chondrocytes. pp38 kinase expression levels increased in a concentration-dependent manner by SSZ but were unaltered in control chondrocytes (p < 0.01). In summary, SSZ significantly inhibited nitric oxide-induced cell death and dedifferentiation, and regulated extracellular regulated kinases 1 and 2 and p38 kinase in rabbit articular chondrocytes.

Keywords: Apoptosis; Chondrocyte; Differentiation; Nitric oxide; Sulfasalazine

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