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Nischarin attenuates apoptosis induced by oxidative stress in PC12 cells

  • Authors:
    • Zhanpeng Guo
    • Yajiang Yuan
    • Yue Guo
    • Hongyu Wang
    • Changwei Song
    • Mina Huang
  • View Affiliations / Copyright

    Affiliations: Department of Orthopedics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China, Department of Nursing, Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China
    Copyright: © Guo et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 663-670
    |
    Published online on: November 27, 2018
       https://doi.org/10.3892/etm.2018.7017
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Abstract

Nischarin (NISCH) is a cytoplasmic protein known to serve an inhibitory role in breast cancer cell apoptosis, migration and invasion. Recently, NISCH has been reported to be involved in the regulation of spinal cord injury (SCI). However, the molecular mechanism is still unclear. Oxidative stress contributes to tissue injury and cell apoptosis during the development of various diseases, including SCI. The aim of the present study was to investigate the role of NISCH in the regulation of apoptosis induced by oxidative stress in PC12 cells. H2O2 was used to establish an oxidative stress model in PC12 cells. Apoptosis levels were examined using flow cytometry analysis, and the expression of NISCH, Bcl‑2, Bcl‑2‑associated X (Bax) and caspase‑3 were examined using western blot and immunofluorescence staining analyses. The results demonstrated that treatment with 100 µM H2O2 significantly increased the apoptotic rate and expression of NISCH in PC12 cells. At 48 h following incubation with 100 µM H2O2, NISCH downregulation partially inhibited apoptosis of PC12 cells. In addition, the expression of Bcl‑2 was significantly reduced and the expression of Bax and caspase‑3 were significantly increased by H2O2 treatment. These effects were also partially inhibited by the downregulation of NISCH. The authors of the present study therefore hypothesize that NISCH may function as a pro‑apoptotic protein that participates in the regulation of oxidative stress, and NISCH downregulation may protect cells from oxidative stress‑induced apoptosis.
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Copy and paste a formatted citation
Spandidos Publications style
Guo Z, Yuan Y, Guo Y, Wang H, Song C and Huang M: Nischarin attenuates apoptosis induced by oxidative stress in PC12 cells. Exp Ther Med 17: 663-670, 2019.
APA
Guo, Z., Yuan, Y., Guo, Y., Wang, H., Song, C., & Huang, M. (2019). Nischarin attenuates apoptosis induced by oxidative stress in PC12 cells. Experimental and Therapeutic Medicine, 17, 663-670. https://doi.org/10.3892/etm.2018.7017
MLA
Guo, Z., Yuan, Y., Guo, Y., Wang, H., Song, C., Huang, M."Nischarin attenuates apoptosis induced by oxidative stress in PC12 cells". Experimental and Therapeutic Medicine 17.1 (2019): 663-670.
Chicago
Guo, Z., Yuan, Y., Guo, Y., Wang, H., Song, C., Huang, M."Nischarin attenuates apoptosis induced by oxidative stress in PC12 cells". Experimental and Therapeutic Medicine 17, no. 1 (2019): 663-670. https://doi.org/10.3892/etm.2018.7017
Copy and paste a formatted citation
x
Spandidos Publications style
Guo Z, Yuan Y, Guo Y, Wang H, Song C and Huang M: Nischarin attenuates apoptosis induced by oxidative stress in PC12 cells. Exp Ther Med 17: 663-670, 2019.
APA
Guo, Z., Yuan, Y., Guo, Y., Wang, H., Song, C., & Huang, M. (2019). Nischarin attenuates apoptosis induced by oxidative stress in PC12 cells. Experimental and Therapeutic Medicine, 17, 663-670. https://doi.org/10.3892/etm.2018.7017
MLA
Guo, Z., Yuan, Y., Guo, Y., Wang, H., Song, C., Huang, M."Nischarin attenuates apoptosis induced by oxidative stress in PC12 cells". Experimental and Therapeutic Medicine 17.1 (2019): 663-670.
Chicago
Guo, Z., Yuan, Y., Guo, Y., Wang, H., Song, C., Huang, M."Nischarin attenuates apoptosis induced by oxidative stress in PC12 cells". Experimental and Therapeutic Medicine 17, no. 1 (2019): 663-670. https://doi.org/10.3892/etm.2018.7017
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