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Article

Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells

  • Authors:
    • Guoliang Ding
    • Jianquan Zhao
    • Dianming Jiang
  • View Affiliations / Copyright

    Affiliations: Department of Orthopedics, First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China
  • Pages: 2553-2560
    |
    Published online on: March 23, 2016
       https://doi.org/10.3892/etm.2016.3179
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Abstract

Osteoporosis is a disease of the skeleton that is characterized by the loss of bone mass and degeneration of bone microstructure, resulting in an increased risk of fracture. Oxidative stress, which is known to promote oxidative damage to mitochondrial function and also cell apoptosis, has been recently indicated to be implicated in osteoporosis. However, there are few agents that counteract oxidative stress in osteoporosis. In the present study, the protective effects of allicin against the oxidative stress‑induced mitochondrial dysfunction and apoptosis were investigated in murine osteoblast‑like MC3T3‑E1 cells. The results demonstrated that allicin counteracted the reduction of cell viability and induction of apoptosis caused by hydrogen peroxide (H2O2) exposure. The inhibition of apoptosis by allicin was confirmed by the inhibition of H2O2‑induced cytochrome c release and caspase‑3 activation. Moreover, the inhibition of apoptosis by allicin was identified to be associated with the counteraction of H2O2‑induced mitochondrial dysfunction. In addition, allicin was demonstrated to be able to significantly ameliorate the repressed phosphoinositide 3-kinase (PI3K)/AKT and cyclic adenosine monophosphate response element-binding protein (CREB)/extracellular-signal-regulated kinase (ERK) signaling pathways by H2O2, which may also be associated with the anti‑oxidative stress effects of allicin. In conclusion, allicin protects osteoblasts from H2O2‑induced oxidative stress and apoptosis in MC3T3‑E1 cells by improving mitochondrial function and the activation of PI3K/AKT and CREB/ERK signaling. The present study implies a promising role of allicin in oxidative stress-associated osteoporosis.
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Copy and paste a formatted citation
Spandidos Publications style
Ding G, Zhao J and Jiang D: Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells. Exp Ther Med 11: 2553-2560, 2016.
APA
Ding, G., Zhao, J., & Jiang, D. (2016). Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells. Experimental and Therapeutic Medicine, 11, 2553-2560. https://doi.org/10.3892/etm.2016.3179
MLA
Ding, G., Zhao, J., Jiang, D."Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells". Experimental and Therapeutic Medicine 11.6 (2016): 2553-2560.
Chicago
Ding, G., Zhao, J., Jiang, D."Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells". Experimental and Therapeutic Medicine 11, no. 6 (2016): 2553-2560. https://doi.org/10.3892/etm.2016.3179
Copy and paste a formatted citation
x
Spandidos Publications style
Ding G, Zhao J and Jiang D: Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells. Exp Ther Med 11: 2553-2560, 2016.
APA
Ding, G., Zhao, J., & Jiang, D. (2016). Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells. Experimental and Therapeutic Medicine, 11, 2553-2560. https://doi.org/10.3892/etm.2016.3179
MLA
Ding, G., Zhao, J., Jiang, D."Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells". Experimental and Therapeutic Medicine 11.6 (2016): 2553-2560.
Chicago
Ding, G., Zhao, J., Jiang, D."Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells". Experimental and Therapeutic Medicine 11, no. 6 (2016): 2553-2560. https://doi.org/10.3892/etm.2016.3179
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