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Article

Chlorogenic acid prevents inflammatory responses in IL‑1β‑stimulated human SW‑1353 chondrocytes, a model for osteoarthritis

  • Authors:
    • Cui‑Cui Liu
    • Yanmin Zhang
    • Bing‑Ling Dai
    • Yu‑Jiao Ma
    • Qian Zhang
    • Yi Wang
    • Hao Yang
  • View Affiliations / Copyright

    Affiliations: Translational Medicine Center, Hong‑Hui Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710054, P.R. China, Department of Pharmacy, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi 710054, P.R. China
  • Pages: 1369-1375
    |
    Published online on: June 6, 2017
       https://doi.org/10.3892/mmr.2017.6698
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Abstract

Chlorogenic acid (CGA), which is a natural compound found in various plants, has been reported to exert notable anti‑inflammatory activities. The present study investigated the effects and underlying mechanism of CGA on interleukin (IL)‑1β‑induced osteoarthritis (OA) chondrocytes. An in vitro OA‑like chondrocyte model was established using IL‑1β‑stimulated human SW‑1353 chondrocytes. Cell viability was assessed using an MTT assay. Nitric oxide (NO) and IL‑6 production were evaluated by Griess reaction and ELISA, respectively. The expression levels of inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2), cyclooxygenase 2 (COX‑2), collagen II, matrix metalloproteinase (MMP)‑13, p65 nuclear factor (NF)‑κB and inhibitor‑κBα were detected by western blot analysis. The results indicated that CGA reversed IL‑1β‑induced increases in iNOS/NO, IL‑6, MMP‑13 and COX‑2/PGE2 production, and reversed the IL‑1β‑mediated downregulation of collagen II. In addition, the data suggested that CGA was capable of inhibiting the IL‑1β‑induced inflammatory response, at least partially via the NF‑κB signaling pathway. In conclusion, CGA may be considered a suitable candidate agent in the treatment of OA.
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Copy and paste a formatted citation
Spandidos Publications style
Liu CC, Zhang Y, Dai BL, Ma YJ, Zhang Q, Wang Y and Yang H: Chlorogenic acid prevents inflammatory responses in IL‑1β‑stimulated human SW‑1353 chondrocytes, a model for osteoarthritis. Mol Med Rep 16: 1369-1375, 2017.
APA
Liu, C., Zhang, Y., Dai, B., Ma, Y., Zhang, Q., Wang, Y., & Yang, H. (2017). Chlorogenic acid prevents inflammatory responses in IL‑1β‑stimulated human SW‑1353 chondrocytes, a model for osteoarthritis. Molecular Medicine Reports, 16, 1369-1375. https://doi.org/10.3892/mmr.2017.6698
MLA
Liu, C., Zhang, Y., Dai, B., Ma, Y., Zhang, Q., Wang, Y., Yang, H."Chlorogenic acid prevents inflammatory responses in IL‑1β‑stimulated human SW‑1353 chondrocytes, a model for osteoarthritis". Molecular Medicine Reports 16.2 (2017): 1369-1375.
Chicago
Liu, C., Zhang, Y., Dai, B., Ma, Y., Zhang, Q., Wang, Y., Yang, H."Chlorogenic acid prevents inflammatory responses in IL‑1β‑stimulated human SW‑1353 chondrocytes, a model for osteoarthritis". Molecular Medicine Reports 16, no. 2 (2017): 1369-1375. https://doi.org/10.3892/mmr.2017.6698
Copy and paste a formatted citation
x
Spandidos Publications style
Liu CC, Zhang Y, Dai BL, Ma YJ, Zhang Q, Wang Y and Yang H: Chlorogenic acid prevents inflammatory responses in IL‑1β‑stimulated human SW‑1353 chondrocytes, a model for osteoarthritis. Mol Med Rep 16: 1369-1375, 2017.
APA
Liu, C., Zhang, Y., Dai, B., Ma, Y., Zhang, Q., Wang, Y., & Yang, H. (2017). Chlorogenic acid prevents inflammatory responses in IL‑1β‑stimulated human SW‑1353 chondrocytes, a model for osteoarthritis. Molecular Medicine Reports, 16, 1369-1375. https://doi.org/10.3892/mmr.2017.6698
MLA
Liu, C., Zhang, Y., Dai, B., Ma, Y., Zhang, Q., Wang, Y., Yang, H."Chlorogenic acid prevents inflammatory responses in IL‑1β‑stimulated human SW‑1353 chondrocytes, a model for osteoarthritis". Molecular Medicine Reports 16.2 (2017): 1369-1375.
Chicago
Liu, C., Zhang, Y., Dai, B., Ma, Y., Zhang, Q., Wang, Y., Yang, H."Chlorogenic acid prevents inflammatory responses in IL‑1β‑stimulated human SW‑1353 chondrocytes, a model for osteoarthritis". Molecular Medicine Reports 16, no. 2 (2017): 1369-1375. https://doi.org/10.3892/mmr.2017.6698
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