Anti-amyloidogenic effects of asarone derivatives from perilla frutescens leaves against beta-amyloid aggregation and nitric oxide productionopen access
- Authors
- Lee J.E.; Kim N.; Yeo J.Y.; Seo D.-G.; Kim S.; Lee J.-S.; Hwang K.W.; Park S.-Y.
- Issue Date
- Dec-2019
- Publisher
- MDPI AG
- Keywords
- Alzheimer's disease; Asarone derivative; Beta-amyloid aggregation; Beta-amyloid disaggregation; Nitric oxide; Perilla frutescens
- Citation
- Molecules, v.24, no.23
- Journal Title
- Molecules
- Volume
- 24
- Number
- 23
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/39060
- DOI
- 10.3390/molecules24234297
- ISSN
- 1420-3049
1420-3049
- Abstract
- Alzheimer's disease (AD) is a progressive, neurodegenerative brain disorder associated with loss of memory and cognitive function. Beta-amyloid (Aβ) aggregates, in particular, are known to be highly neurotoxic and lead to neurodegeneration. Therefore, blockade or reduction of Aβ aggregation is a promising therapeutic approach in AD. We have previously reported an inhibitory effect of the methanol extract of Perilla frutescens (L.) Britton (Lamiaceae) and its hexane fraction on Aβ aggregation. Here, the hexane fraction of P. frutescens was subjected to diverse column chromatography based on activity-guided isolation methodology. This approach identified five asarone derivatives including 2,3-dimethoxy-5-(1E)-1-propen-1-yl-phenol (1), β-asarone (2), 3- (2,4,5-trimethoxyphenyl)-(2E)-2-propen-1-ol (3), asaronealdehyde (4), and α-asarone (5). All five asarone derivatives efficiently reduced the aggregation of Aβ and disaggregated preformed Aβ aggregates in a dose-dependent manner as determined by a Thioflavin T (ThT) fluorescence assay. Furthermore, asarone derivatives protected PC12 cells from Aβ aggregate-induced toxicity by reducing the aggregation of Aβ, and significantly reduced NO production from LPS-stimulated BV2 microglial cells. Taken together, these results suggest that asarone derivatives derived from P. frutescens are neuroprotective and have the prophylactic and therapeutic potential in AD. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
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