Naringenin reduces oxidative stress and improves mitochondrial dysfunction via activation of the Nrf2/ARE signaling pathway in neurons

  • Authors:
    • Kaihua Wang
    • Zhenzhen Chen
    • Longjian Huang
    • Bing Meng
    • Xinmei Zhou
    • Xiaodong Wen
    • Ding Ren
  • View Affiliations

  • Published online on: September 13, 2017     https://doi.org/10.3892/ijmm.2017.3134
  • Pages: 1582-1590
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Abstract

Oxidative stress and mitochondrial dysfunction are considered to be major contributing factors in the development and progression of many neurodegenerative diseases. Naringenin (NAR) is an abundant flavanone in the Citrus genus and has been found to exert antioxidant, anticarcinogenic and antimutagenic effects. However, the potential underlying mechanism of its antioxidant effects remains unclear. In the present study, the authors investigated the antioxidant effect of NAR on neurons in vitro. Neurons isolated from the brains of Sprague-Dawley rats were randomly divided into a control group, model group, NAR-L group, NAR-M group and NAR-H group. The model group received hypoxia and re-oxygenation treatment, and the NAR-L, NAR-M and NAR-H groups received 20, 40 and 80 µM NAR, respectively. The levels of reactive oxygen species (ROS) in each group were detected by chloromethyl-2',7'dichlorodihydro fluorescein diacetate staining, and differences in mitochondrial dysfunction were analyzed through measurement of mitochondrial membrane potential (∆ψm), adenine nucleotide translocase transport activity and adenine nucleotide levels. MTT and flow cytometry assays were also used to analyze cell proliferation and apoptosis, and the effects of NAR on the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway were investigated using small interfering RNA methods. The authors detected an increased accumulation of ROS in the model group, and high-dose NAR could significantly reduce the levels of ROS. Furthermore, NAR could improve mitochondrial dysfunction, as indicated by increased levels of high-energy phosphates, enhanced mitochondrial ANT transport activity and increased mitochondrial membrane potential. Moreover, NAR increased cell viability and decreased the rate of cell apoptosis. NAR also increased the expression of Nrf2 and its downstream target genes. These findings demonstrated that NAR could reduce oxidative stress and improve mitochondrial dysfunction via activation of the Nrf2/ARE signaling pathway in neurons.
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November-2017
Volume 40 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Wang K, Chen Z, Huang L, Meng B, Zhou X, Wen X and Ren D: Naringenin reduces oxidative stress and improves mitochondrial dysfunction via activation of the Nrf2/ARE signaling pathway in neurons. Int J Mol Med 40: 1582-1590, 2017
APA
Wang, K., Chen, Z., Huang, L., Meng, B., Zhou, X., Wen, X., & Ren, D. (2017). Naringenin reduces oxidative stress and improves mitochondrial dysfunction via activation of the Nrf2/ARE signaling pathway in neurons. International Journal of Molecular Medicine, 40, 1582-1590. https://doi.org/10.3892/ijmm.2017.3134
MLA
Wang, K., Chen, Z., Huang, L., Meng, B., Zhou, X., Wen, X., Ren, D."Naringenin reduces oxidative stress and improves mitochondrial dysfunction via activation of the Nrf2/ARE signaling pathway in neurons". International Journal of Molecular Medicine 40.5 (2017): 1582-1590.
Chicago
Wang, K., Chen, Z., Huang, L., Meng, B., Zhou, X., Wen, X., Ren, D."Naringenin reduces oxidative stress and improves mitochondrial dysfunction via activation of the Nrf2/ARE signaling pathway in neurons". International Journal of Molecular Medicine 40, no. 5 (2017): 1582-1590. https://doi.org/10.3892/ijmm.2017.3134