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Article

Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells

  • Authors:
    • Li Yan
    • Rui Hu
    • Song Tu
    • Wen‑Jun Cheng
    • Qiong Zheng
    • Jun‑Wen Wang
    • Wu‑Sheng Kan
    • Yi‑Jun Ren
  • View Affiliations / Copyright

    Affiliations: Department of Reparative and Reconstructive Surgery of Orthopedics, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430033, P.R. China
  • Pages: 1981-1985
    |
    Published online on: July 21, 2016
       https://doi.org/10.3892/ol.2016.4902
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Abstract

Previously, the application of cisplatin in chemotherapy was limited due to the significant side effects on normal cell growth. In the present study, the concomitant application of emodin with cisplatin was demonstrated to ameliorate cisplatin‑induced oxidative stress and markedly suppress tumor cell proliferation for the first time. Human osteosarcoma MG-63 cells were treated with cisplatin alone or in combination with emodin. The cell viability was determined by MTS assays and the augmentation of reactive oxygen species were determined by fluorogenic probes; in addition, a stable MG‑63 subline bearing antioxidant response element (ARE)‑driven luciferase expression was developed to monitor the activation of the nuclear factor erythroid 2‑related factor 2 (Nrf2)‑ARE signaling pathway. The results indicated that cisplatin or emodin may inhibit MG‑63 cell proliferation in a time‑ or dose‑dependent manner, respectively. Concomitant treatment with cisplatin and emodin demonstrated synergic anti‑tumor effects. Cisplatin augmented reactive oxygen species in the MG‑63 cells, followed by the translocation of Nrf2 from the cytoplasm into the nucleus, which triggered ARE‑driven luciferase expression. The addition of emodin diminished the previously described phenomenon, resulting in decreased ROS augmentation, translocation of Nrf2 and ARE‑driven luciferase activity. In conclusion, emodin could ameliorate cisplatin‑induced oxidative stress and protect the cells from oxidative stress-induced damage. The findings of the present study provide a novel strategy for the treatment of osteosarcoma using emodin and cisplatin.
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Copy and paste a formatted citation
Spandidos Publications style
Yan L, Hu R, Tu S, Cheng WJ, Zheng Q, Wang JW, Kan WS and Ren YJ: Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells. Oncol Lett 12: 1981-1985, 2016.
APA
Yan, L., Hu, R., Tu, S., Cheng, W., Zheng, Q., Wang, J. ... Ren, Y. (2016). Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells. Oncology Letters, 12, 1981-1985. https://doi.org/10.3892/ol.2016.4902
MLA
Yan, L., Hu, R., Tu, S., Cheng, W., Zheng, Q., Wang, J., Kan, W., Ren, Y."Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells". Oncology Letters 12.3 (2016): 1981-1985.
Chicago
Yan, L., Hu, R., Tu, S., Cheng, W., Zheng, Q., Wang, J., Kan, W., Ren, Y."Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells". Oncology Letters 12, no. 3 (2016): 1981-1985. https://doi.org/10.3892/ol.2016.4902
Copy and paste a formatted citation
x
Spandidos Publications style
Yan L, Hu R, Tu S, Cheng WJ, Zheng Q, Wang JW, Kan WS and Ren YJ: Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells. Oncol Lett 12: 1981-1985, 2016.
APA
Yan, L., Hu, R., Tu, S., Cheng, W., Zheng, Q., Wang, J. ... Ren, Y. (2016). Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells. Oncology Letters, 12, 1981-1985. https://doi.org/10.3892/ol.2016.4902
MLA
Yan, L., Hu, R., Tu, S., Cheng, W., Zheng, Q., Wang, J., Kan, W., Ren, Y."Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells". Oncology Letters 12.3 (2016): 1981-1985.
Chicago
Yan, L., Hu, R., Tu, S., Cheng, W., Zheng, Q., Wang, J., Kan, W., Ren, Y."Emodin mitigates the oxidative stress induced by cisplatin in osteosarcoma MG63 cells". Oncology Letters 12, no. 3 (2016): 1981-1985. https://doi.org/10.3892/ol.2016.4902
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