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Article

Paeoniflorin inhibits IL-1β-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway

  • Authors:
    • Peng-Fei Hu
    • Wei-Ping Chen
    • Jia-Peng Bao
    • Li-Dong Wu
  • View Affiliations / Copyright

    Affiliations: Department of Orthopaedic Surgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, P.R. China
  • Pages: 6194-6200
    |
    Published online on: February 26, 2018
       https://doi.org/10.3892/mmr.2018.8631
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Abstract

Apoptosis serves a pivotal role in the pathogenesis of osteoarthritis (OA). Increasing evidence has demonstrated that paeoniflorin exerts key properties (including anticancer, anti-inflammation and neuroprotective) for clinical applications. However, the precise role of paeoniflorin in articular cartilage apoptosis remains unknown. The present study explored the effects and potential molecular mechanism of paeoniflorin on rat chondrocyte apoptosis. Rat articular chondrocytes were cultured in monolayers. The lactate dehydrogenase (LDH) release rate of cells was determined by an LDH release assay. Annexin V-fluorescein isothiocyanate and propidium iodide staining were performed to detect early and advanced apoptotic cells by flow cytometry. The activity of caspase-3 in chondrocytes was determined using a caspase-3 activity assay. The expression of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) was examined by reverse transcription‑quantitative polymerase chain and western blotting. The present study also examined the protein kinase B (Akt) signaling pathway by western blotting. Treatment with 25 or 50 µM paeoniflorin markedly decreased the release of LDH and the ratio of apoptotic cells in interleukin (IL)-1β-induced rat chondrocytes. Paeoniflorin treatment decreased the mRNA and protein levels of Bax, and increased the level of Bcl-2. Paeoniflorin also reduced the activity of caspase-3 in chondrocytes. Furthermore, paeoniflorin was determined to regulate the Akt signaling pathway by increasing Akt phosphorylation. Therefore, paeoniflorin may exert its protective effect by inhibiting apoptosis in IL-1β-induced rat chondrocytes and thus, may be an effective agent in the prevention and treatment of OA.
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Copy and paste a formatted citation
Spandidos Publications style
Hu P, Chen W, Bao J and Wu L: Paeoniflorin inhibits IL-1β-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway. Mol Med Rep 17: 6194-6200, 2018.
APA
Hu, P., Chen, W., Bao, J., & Wu, L. (2018). Paeoniflorin inhibits IL-1β-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway. Molecular Medicine Reports, 17, 6194-6200. https://doi.org/10.3892/mmr.2018.8631
MLA
Hu, P., Chen, W., Bao, J., Wu, L."Paeoniflorin inhibits IL-1β-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway". Molecular Medicine Reports 17.4 (2018): 6194-6200.
Chicago
Hu, P., Chen, W., Bao, J., Wu, L."Paeoniflorin inhibits IL-1β-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway". Molecular Medicine Reports 17, no. 4 (2018): 6194-6200. https://doi.org/10.3892/mmr.2018.8631
Copy and paste a formatted citation
x
Spandidos Publications style
Hu P, Chen W, Bao J and Wu L: Paeoniflorin inhibits IL-1β-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway. Mol Med Rep 17: 6194-6200, 2018.
APA
Hu, P., Chen, W., Bao, J., & Wu, L. (2018). Paeoniflorin inhibits IL-1β-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway. Molecular Medicine Reports, 17, 6194-6200. https://doi.org/10.3892/mmr.2018.8631
MLA
Hu, P., Chen, W., Bao, J., Wu, L."Paeoniflorin inhibits IL-1β-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway". Molecular Medicine Reports 17.4 (2018): 6194-6200.
Chicago
Hu, P., Chen, W., Bao, J., Wu, L."Paeoniflorin inhibits IL-1β-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway". Molecular Medicine Reports 17, no. 4 (2018): 6194-6200. https://doi.org/10.3892/mmr.2018.8631
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