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Am J Chin Med. 2016;44(7):1325-1347. Epub 2016 Oct 25.

Coriandrum sativum Suppresses Aβ42-Induced ROS Increases, Glial Cell Proliferation, and ERK Activation.

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* Department of Oriental Medicine, Dongguk University, Gyeogju 38066, Republic of Korea.
† Department of Oriental Neuropsychiatry, Graduate School of Oriental Medicine, Republic of Korea.
‡ Department of Biological Sciences, Konkuk University, Seoul 05029, Republic of Korea.
§ College of Pharmacy and BK21PLUS R-FIND Team, Dongguk University, Goyang 10326, Republic of Korea.
¶ Neurophysiology Research Group, Bio-Nano Research Centre, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Republic of Korea.
∥ Korea Hemp Institute, Konkuk University, Seoul 0529, Republic of Korea.
** Department of Brain and Cognitive Sciences, DGIST, Daegu 42988, Republic of Korea.
†† Dongguk University Research Institute of Biotechnology, Dongguk University, Seoul 04620, Republic of Korea.


Alzheimer's disease (AD), the most common neurodegenerative disease, has a complex and widespread pathology that is characterized by the accumulation of amyloid [Formula: see text]-peptide (A[Formula: see text]) 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 A[Formula: see text] 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 A[Formula: see text]-treated mammalian cells and [Formula: see text]42-expressing flies. Moreover, C. sativum extract intake suppressed [Formula: see text]-induced cell death in the larval imaginal disc and brain without affecting A[Formula: see text]42 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 A[Formula: see text]-induced phosphorylation of extracellular signal-regulated kinase (ERK). The constitutively active form of ERK abolished the protective function of C. sativum extract against the [Formula: see text]-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.


Alternative Medicine; Alzheimer’s Disease; Amyloid -Peptide; Animal Models; Coriandrum sativum; Extracellular Signal-Regulated Kinase

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