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  4. Neuroprotective effects of several phytochemicals from Angelica Sinensis Radix and seed embryo of Nelumbo nucifera Gaertn against Aβ1-42-induced toxicity in rat cortical neurons
 
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Neuroprotective effects of several phytochemicals from Angelica Sinensis Radix and seed embryo of Nelumbo nucifera Gaertn against Aβ1-42-induced toxicity in rat cortical neurons

Date Issued
2011
Date
2011
Author(s)
Tsai, I-Chieh
URI
http://ntur.lib.ntu.edu.tw//handle/246246/248231
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline in memory, orientation, judgment, and reasoning; it is also the most common form of dementia among the elderly people. Pathologically, AD is manifested by oxidative stress induced neuronal cell death, deposition of amyloid-β (Aβ) peptide into senile plaques in the extracellular space, and formation of neurofibrillary tangles inside the neurons. Recent studies suggest that soluble Aβ oligomers may be the primary toxic species in AD. Therefore, the objective of this study is to find the potential phytochemicals that can protect neuron against Aβ oligomer induced toxicity. Flavonoids, a large group of natural compounds, have been proven to possess neuroprotective effects through its antioxidative ability. Flavonoids isolated from lotus (Nelumbo nucifera) seed embryo were identified to be orientin. isoorientin, isoquercirtrin and hyperoside. Also, Z-ligustilide is an active compound in Angelica sinensis. Using Ginkgo biloba extract (EGb761) as positive control, we plan on tesing the above phytochemicals for the potential neuroprotective effect against Aβ1-42 induced toxicity in primary rat cortical neurons. According to the results of cell viability assessed by the MTT colorimetric assay, the most effective dose of isoorientin and isoquercitrin is 5 μM, and Z-ligustlie、orientin and hyperoside is 25 μM. The protctive effect are as follows: orientin > Z-ligustlie > isoorientin > hyperoside > isoquercitrin. In dot blot assay, only EGb761 was found to inhibit the Aβ1-42 fibrillization, indicating that these compounds may protect neuron through accelerating Aβ assembly.
Subjects
Alzheimer’s disease (AD)
amyloid-β (Aβ) peptide
primary rat cortical neuron
Type
thesis
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