Open Access

Aminoguanidine inhibits IL‑1β‑induced protein expression of iNOS and COX‑2 by blocking the NF‑κB signaling pathway in rat articular chondrocytes

  • Authors:
    • Yuanqiang Ma
    • Xiaopeng Song
    • Tianwen Ma
    • Yue Li
    • Hui Bai
    • Zhiheng Zhang
    • Hailong Hu
    • Rui Yuan
    • Yajing Wen
    • Li Gao
  • View Affiliations

  • Published online on: July 17, 2020     https://doi.org/10.3892/etm.2020.9021
  • Pages: 2623-2630
  • Copyright: © Ma et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Osteoarthritis is a chronic joint disease which has a serious impact on the health and quality of life of affected humans and animals. As an inhibitor of inducible nitric oxide synthase (iNOS), aminoguanidine (AG) displays anti‑inflammatory effects. The purpose of the present study was to investigate the effect of AG on the expression of iNOS and cyclooxygenase‑2 (COX‑2), and the activity of the NF‑κB signaling pathway in rat chondrocytes stimulated by interleukin‑1β (IL‑1β). The viability of chondrocytes treated with AG (0.3, 1 or 3 mM) alone was determined using a Cell Counting Kit‑8 assay. Subsequently, the chondrocytes were treated with either 10 ng/ml IL‑1β alone, or co‑treated with increasing concentrations of AG (0.3, 1 or 3 mM) and 10 ng/ml IL‑1β. The protein levels of COX‑2, iNOS, phosphorylated (p)‑p65, p65, p‑NF‑κβ inhibitor α (IκBα), IκBα, p‑inhibitor of NF‑κβ‑β (IKKβ) and IKKβ were evaluated by western blotting. NF‑κB translocation was determined by immunofluorescence analysis. Western blotting and reverse transcription‑quantitative PCR were used to detect expression levels of relevant proteins/genes. The results suggested that the inhibitory effect of AG on the protein and gene expression levels of iNOS and COX‑2 in IL‑1β‑treated chondrocytes was dose‑dependent. In addition, AG decreased the level of phosphorylation of IKKβ, IκBα and NF‑κB p65, the degradation of IKKβ, IκBα and p65, and the translocation of NF‑κB in IL‑1β‑stimulated chondrocytes. The most significant inhibitory effect of AG was observed at a concentration of 1 mM. Therefore, the present study suggested that AG may serve as a potential agent to reduce the inflammatory response of chondrocytes stimulated by IL‑1β.

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September-2020
Volume 20 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Ma Y, Song X, Ma T, Li Y, Bai H, Zhang Z, Hu H, Yuan R, Wen Y, Gao L, Gao L, et al: Aminoguanidine inhibits IL‑1β‑induced protein expression of iNOS and COX‑2 by blocking the NF‑κB signaling pathway in rat articular chondrocytes. Exp Ther Med 20: 2623-2630, 2020
APA
Ma, Y., Song, X., Ma, T., Li, Y., Bai, H., Zhang, Z. ... Gao, L. (2020). Aminoguanidine inhibits IL‑1β‑induced protein expression of iNOS and COX‑2 by blocking the NF‑κB signaling pathway in rat articular chondrocytes. Experimental and Therapeutic Medicine, 20, 2623-2630. https://doi.org/10.3892/etm.2020.9021
MLA
Ma, Y., Song, X., Ma, T., Li, Y., Bai, H., Zhang, Z., Hu, H., Yuan, R., Wen, Y., Gao, L."Aminoguanidine inhibits IL‑1β‑induced protein expression of iNOS and COX‑2 by blocking the NF‑κB signaling pathway in rat articular chondrocytes". Experimental and Therapeutic Medicine 20.3 (2020): 2623-2630.
Chicago
Ma, Y., Song, X., Ma, T., Li, Y., Bai, H., Zhang, Z., Hu, H., Yuan, R., Wen, Y., Gao, L."Aminoguanidine inhibits IL‑1β‑induced protein expression of iNOS and COX‑2 by blocking the NF‑κB signaling pathway in rat articular chondrocytes". Experimental and Therapeutic Medicine 20, no. 3 (2020): 2623-2630. https://doi.org/10.3892/etm.2020.9021