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    Protective effects of onion-derived quercetin on glutamate-mediated hippocampal neuronal cell death

    Eun-Ju Yang1, Geum-Soog Kim2, Jeong Ah Kim3, Kyung-Sik Song3★★ Corresponding author

    1. 1BK21 Research Team for Developing Functional Health and Food Materials, College of Agriculture and Life Sciences, Kyungpook National University, Daegu 702-701.
    2. 2Department of Herbal Crop Research, National Institute of Horticultural & Herbal Science, RDA, Eumseong 369-873.
    3. 3Research Institute of Pharmaceutical Sciences, College of Pharmacy, Kyungpook National University, Daegu 702-701, Republic of Korea.

    CORRESPONDENCE

    Kyung-Sik Song

    Research Institute of Pharmaceutical Sciences, College of Pharmacy, Kyungpook National University, Daegu 702-701, Republic of Korea.

    kssong@knu.ac.kr

    Received: 21-09-2012; Revised: 11-11-2012.

    Volume 9, Issue 36 · pp. 302–308 · PUBLISHED 7 September 2013 · DOI: 10.4103/0973-1296.117824

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Background: Neurodegenerative diseases are characterized by progressive neuron degeneration in specifi c functional systems of the central or peripheral nervous system. This study investigated the protective effects of quercetin isolated from onion on neuronal cells and its protective mechanisms against glutamate-induced apoptosis in HT22 cells. Materials and Methods: HT22 cells were cultured to study the neuroprotective mechanism of quercetin against glutamate-mediated oxidative stress. The intracellular reactive oxygen species (ROS) level and mitochondrial membrane potential (∆m) were measured. The protein expression of calpain, spectrin, Bcl-2, Bax, Bid, cytochrome c, and mitogen-activated protein kinases (MAPKs) was evaluated by Western blotting. Results: Quercetin had a protective effect by reducing both intracellular ROS overproduction and glutamate-mediated Ca2+ infl ux. These effects were due to the downregulation of several apoptosis-related biochemical markers. Calpain expression was reduced and spectrin cleavage was inhibited by quercetin in glutamate-exposed HT22 cells. Disruption of the mitochondrial membrane potential (∆m), activation of the pro-apoptotic proteins Bid and Bax, and cytochrome c release in response to glutamate-induced oxidative stress were reduced. Quercetin also suppressed phosphorylation of MAPKs. Conclusion: This is the fi rst report on the detailed mechanisms of the protective effect of quercetin on HT22 cells. Onion extract and quercetin may be useful for preventing or treating neurodegenerative disorders.

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      Yang, E., Kim, G., Kim, J. A., & Song, K. (2013). Protective effects of onion-derived quercetin on glutamate-mediated hippocampal neuronal cell death. Pharmacognosy Magazine, 9(36), 302–308. https://doi.org/10.4103/0973-1296.117824