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Neuroprotective effect of Aster yomena (Kitam.) Honda against hydrogen peroxide-induced oxidative stress in SH-SY5Y cells

  • Kim, Min Jeong (Department of Food Science and Nutrition, Pusan National University) ;
  • Kim, Ji Hyun (Department of Food Science, Gyeongnam National University of Science and Technology) ;
  • Lee, Sanghyun (Department of Plant Science and Technology, Chung-Ang University) ;
  • Cho, Eun Ju (Department of Food Science and Nutrition, Pusan National University) ;
  • Kim, Hyun Young (Department of Food Science, Gyeongnam National University of Science and Technology)
  • Received : 2020.08.06
  • Accepted : 2020.09.17
  • Published : 2020.09.30

Abstract

Oxidative stress is one of the contributors of neurodegenerative disorders including Alzheimer's disease. According to previous studies, Aster yomena (Kitam.) Honda (AY) possesses variable pharmacological activities including anti-coagulant and anti-obesity effect. In this study, we aimed to determine the neuroprotective effect of ethyl acetate fraction from Aster yomena (Kitam.) Honda (EFAY) against oxidative stress. Therefore, we carried out 3-(4,5-dimethylthiazol-2-yl)-2,3-diphenyl tetrazolium bromide, lactate dehydrogenase (LDH), and 2',7'-dichlorofluorescin diacetate assays in SH-SY5Y neuronal cells treated with hydrogen peroxide (H2O2). H2O2-treated control cells exhibited reduced viability of cells, and increased LDH release and reactive oxygen species (ROS) production compared to normal cells. However, treatment with EFAY restored the cell viability and inhibited LDH release and ROS production. To investigate the underlying mechanisms by which EFAY attenuated neuronal oxidative damage, we measured protein expressions using Western blot analysis. Consequently, it was observed that EFAY down-regulated cyclooxygenase-2 and interleukin-1β protein expressions in H2O2-treated SH-SY5Y cells that mediated inflammatory reaction. In addition, apoptosis-related proteins including B-cell lymphoma-2-associated X protein/B-cell lymphoma-2 ratio, cleaved caspase-9, and cleaved-poly (ADP-ribose) polymerase protein expressions were suppressed when H2O2-treated cells were exposed to EFAY. Our results indicate that EFAY ameliorated H2O2-induced neuronal damage by regulating inflammation and apoptosis. Altogether, AY could be potential therapeutic agent for neurodegenerative diseases.

Keywords

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