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Article

β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration

  • Authors:
    • Feng Wen
    • Jun Yu
    • Cheng‑Jian He
    • Zhi‑Wen Zhang
    • Ao‑Fei Yang
  • View Affiliations / Copyright

    Affiliations: Department of Traditional Chinese Traumatology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, Hubei 430061, P.R. China, Department of Osteology, Xiaogan No. 1 People's Hospital, Xiaogan, Hubei 432001, P.R. China
  • Pages: 2440-2448
    |
    Published online on: January 15, 2019
       https://doi.org/10.3892/mmr.2019.9861
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Abstract

Increasing cell apoptosis is one of the major causes of intervertebral disc degeneration (IDD). β-ecdysterone has been demonstrated to protect PC12 cells against neurotoxicity. A previous study revealed that β‑ecdysterone may be involved in the regulation of autophagy in osteoblasts. Therefore, we hypothesized that β‑ecdysterone may possess therapeutic effects on IDD via autophagy stimulation. The effect of β‑ecdysterone on IDD was explored by in vitro experiments. The results demonstrated that β‑ecdysterone attenuated the apoptosis induced by tert‑butyl hydroperoxide via promoting autophagy in nucleus pulposus cells. Beclin‑1, an indispensable protein for the stimulation of autophagy, is upregulated and stabilized by β‑ecdysterone in a dose‑ and time‑dependent manner in nucleus pulposus cells. Inhibition of autophagy with 3‑methyladenine partially abrogated the protective function of β‑ecdysterone against apoptosis of nucleus pulposus cells, indicating that autophagy participated in the protective effect of β‑ecdysterone on IDD. Additionally, β‑ecdysterone promoted the expression of anabolic genes while inhibiting the expression of catabolic genes in nucleus pulposus cells. Collectively, the present study demonstrated that β‑ecdysterone may protect nucleus pulposus cells against apoptosis by autophagy stimulation and ameliorate disc degeneration, which indicates that β‑ecdysterone may be a potential therapeutic agent for IDD.
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Copy and paste a formatted citation
Spandidos Publications style
Wen F, Yu J, He CJ, Zhang ZW and Yang AF: β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration. Mol Med Rep 19: 2440-2448, 2019.
APA
Wen, F., Yu, J., He, C., Zhang, Z., & Yang, A. (2019). β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration. Molecular Medicine Reports, 19, 2440-2448. https://doi.org/10.3892/mmr.2019.9861
MLA
Wen, F., Yu, J., He, C., Zhang, Z., Yang, A."β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration". Molecular Medicine Reports 19.3 (2019): 2440-2448.
Chicago
Wen, F., Yu, J., He, C., Zhang, Z., Yang, A."β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration". Molecular Medicine Reports 19, no. 3 (2019): 2440-2448. https://doi.org/10.3892/mmr.2019.9861
Copy and paste a formatted citation
x
Spandidos Publications style
Wen F, Yu J, He CJ, Zhang ZW and Yang AF: β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration. Mol Med Rep 19: 2440-2448, 2019.
APA
Wen, F., Yu, J., He, C., Zhang, Z., & Yang, A. (2019). β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration. Molecular Medicine Reports, 19, 2440-2448. https://doi.org/10.3892/mmr.2019.9861
MLA
Wen, F., Yu, J., He, C., Zhang, Z., Yang, A."β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration". Molecular Medicine Reports 19.3 (2019): 2440-2448.
Chicago
Wen, F., Yu, J., He, C., Zhang, Z., Yang, A."β‑ecdysterone protects against apoptosis by promoting autophagy in nucleus pulposus cells and ameliorates disc degeneration". Molecular Medicine Reports 19, no. 3 (2019): 2440-2448. https://doi.org/10.3892/mmr.2019.9861
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