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Coriandrum sativum Suppresses A beta 42-Induced ROS Increases, Glial Cell Proliferation, and ERK Activation

Coriandrum sativum Suppresses A beta 42-Induced ROS Increases, Glial Cell Proliferation, and ERK Activation
Liu, QF[Liu, Quan Feng]Jeong, H[Jeong, Haemin]Lee, JH[Lee, Jang Ho]Hong, YK[Hong, Yoon Ki]Oh, Y[Oh, Youngje]Kim, YM[Kim, Young-Mi]Suh, YS[Suh, Yoon Seok]Bang, S[Bang, Semin]Yun, HS[Yun, Hye Sup]Lee, K[Lee, Kyungho]Cho, SM[Cho, Sung Man]Lee, SB[Lee, Sung Bae]Jeon, S[Jeon, Songhee]Chin, YW[Chin, Young-Won]Koo, BS[Koo, Byung-Soo]Cho, KS[Cho, Kyoung Sang]
DGIST Authors
Lee, SB[Lee, Sung Bae]
Issue Date
American Journal of Chinese Medicine, 44(7), 1325-1347
Article Type
Alternative MedicineAlzheimer&aposs Disease (AD)Amyloid-Beta (A Beta) -PeptideAnimal ModelsCoriandrum SativumExtracellular Signal-Regulated Kinase
Alzheimer's disease (AD), the most common neurodegenerative disease, has a complex and widespread pathology that is characterized by the accumulation of amyloid β-peptide (Aβ) in the brain and various cellular abnormalities, including increased oxidative damage, an amplified inflammatory response, and altered mitogen-activated protein kinase signaling. Based on the complex etiology of AD, traditional medicinal plants with multiple effective components are alternative treatments for patients with AD. In the present study, we investigated the neuroprotective effects of an ethanol extract of Coriandrum sativum (C. sativum) leaves on Aβ cytotoxicity and examined the molecular mechanisms underlying the beneficial effects. Although recent studies have shown the benefits of the inhalation of C. sativum oil in an animal model of AD, the detailed molecular mechanisms by which C. sativum exerts its neuroprotective effects are unclear. Here, we found that treatment with C. sativum extract increased the survival of both Aβ-treated mammalian cells and Aβ42-expressing flies. Moreover, C. sativum extract intake suppressed Aβ42-induced cell death in the larval imaginal disc and brain without affecting Aβ42 expression and accumulation. Interestingly, the increases in reactive oxygen species levels and glial cell number in AD model flies were reduced by C. sativum extract intake. Additionally, C. sativum extract inhibited the epidermal growth factor receptor- and Aβ-induced phosphorylation of extracellular signal-regulated kinase (ERK). The constitutively active form of ERK abolished the protective function of C. sativum extract against the Aβ42-induced eye defect phenotype in Drosophila. Taken together, these results suggest that C. sativum leaves have antioxidant, anti-inflammatory, and ERK signaling inhibitory properties that are beneficial for patients with AD. © 2016 World Scientific Publishing Company.
World Scientific Publishing
Related Researcher
  • Author Lee, Sung-Bae SB LAB(Lab of Neurodegenerative diseases and Aging)
  • Research Interests Cellular mechanism of neurodegenerative diseases; Neuronal maintenance and remodeling; 퇴행성 뇌질환의 세포기전; 신경계 유지 및 리모델링 연구
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Department of Brain and Cognitive SciencesSB LAB(Lab of Neurodegenerative diseases and Aging)1. Journal Articles

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