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Salidroside prevents hydroperoxide‑induced oxidative stress and apoptosis in retinal pigment epithelium cells

  • Authors:
    • Yan Yin
    • Dejie Liu
    • Donghua Tian
  • View Affiliations / Copyright

    Affiliations: Department of Ophthalmology, Jining No. 1 People's Hospital, Jining, Shandong 272011, P.R. China, Department of Ophthalmology, Yantai Yeda Hospital, Yantai, Shandong 264006, P.R. China
    Copyright: © Yin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2363-2368
    |
    Published online on: July 20, 2018
       https://doi.org/10.3892/etm.2018.6494
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Abstract

Salidroside (SAL) is the major pharmacologically active constituent of Rhodiola rosea, which possesses a wide range of pharmacological functions, including anti‑aging, anti‑inflammatory, antioxidant, anticancer and neuroprotective activities. However, the effects and mechanisms of SAL on oxidative stress in retinal pigment epithelial (RPE) cells exposed to hydrogen peroxide (H2O2) remain unclear. The present study investigated the protective effects of SAL and the underlying mechanisms against H2O2‑induced oxidative stress in human RPE cells. ARPE‑19 cells were treated with various doses of SAL for 24 h and then exposed to 200 µM H2O2 for 24 h. Cell viability was analyzed by a MTT assay, and the intracellular levels of reactive oxygen species were measured using CellROX orange reagent. Cell apoptosis was analyzed by annexin V/propidium iodide double staining, followed by flow cytometry. The levels of B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein, phospho (p)‑protein kinase B (Akt), Akt, p‑glycogen synthase kinase (GSK)‑3β and GSK‑3β were evaluated using western blotting. The results demonstrated that SAL markedly attenuated H2O2‑induced loss of cell viability. SAL also ameliorated H2O2‑induced oxidative stress and cell apoptosis in RPE cells. In addition, pretreatment with SAL significantly increased the phosphorylation levels of Akt and GSK‑3β in H2O2‑treated ARPE‑19 cells. In conclusion, the present study demonstrated that SAL protected RPE cells against H2O2‑induced cell injury through the activation of the Akt/GSK‑3β signaling pathway. This suggests that SAL may be a potential therapeutic strategy for the treatment of age‑related macular degeneration.
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Copy and paste a formatted citation
Spandidos Publications style
Yin Y, Liu D and Tian D: Salidroside prevents hydroperoxide‑induced oxidative stress and apoptosis in retinal pigment epithelium cells. Exp Ther Med 16: 2363-2368, 2018.
APA
Yin, Y., Liu, D., & Tian, D. (2018). Salidroside prevents hydroperoxide‑induced oxidative stress and apoptosis in retinal pigment epithelium cells. Experimental and Therapeutic Medicine, 16, 2363-2368. https://doi.org/10.3892/etm.2018.6494
MLA
Yin, Y., Liu, D., Tian, D."Salidroside prevents hydroperoxide‑induced oxidative stress and apoptosis in retinal pigment epithelium cells". Experimental and Therapeutic Medicine 16.3 (2018): 2363-2368.
Chicago
Yin, Y., Liu, D., Tian, D."Salidroside prevents hydroperoxide‑induced oxidative stress and apoptosis in retinal pigment epithelium cells". Experimental and Therapeutic Medicine 16, no. 3 (2018): 2363-2368. https://doi.org/10.3892/etm.2018.6494
Copy and paste a formatted citation
x
Spandidos Publications style
Yin Y, Liu D and Tian D: Salidroside prevents hydroperoxide‑induced oxidative stress and apoptosis in retinal pigment epithelium cells. Exp Ther Med 16: 2363-2368, 2018.
APA
Yin, Y., Liu, D., & Tian, D. (2018). Salidroside prevents hydroperoxide‑induced oxidative stress and apoptosis in retinal pigment epithelium cells. Experimental and Therapeutic Medicine, 16, 2363-2368. https://doi.org/10.3892/etm.2018.6494
MLA
Yin, Y., Liu, D., Tian, D."Salidroside prevents hydroperoxide‑induced oxidative stress and apoptosis in retinal pigment epithelium cells". Experimental and Therapeutic Medicine 16.3 (2018): 2363-2368.
Chicago
Yin, Y., Liu, D., Tian, D."Salidroside prevents hydroperoxide‑induced oxidative stress and apoptosis in retinal pigment epithelium cells". Experimental and Therapeutic Medicine 16, no. 3 (2018): 2363-2368. https://doi.org/10.3892/etm.2018.6494
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