Lavender and coriander essential oils and their main component linalool exert a protective effect against amyloid‐β neurotoxicity. (12th August 2020)

• Record Type: Journal Article
• Authors: Caputo, Lucia; Piccialli, Ilaria; Ciccone, Roselia; de Caprariis, Paolo; Massa, Antonio; De Feo, Vincenzo; Pannaccione, Anna
• Is Part Of: Phytotherapy research. Volume 35:Number 1(2021)
• Page Start: 486
• Page End: 493
• Publication Date: 2020-08-12
• Subjects: Alzheimer's disease -- amyloid‐β oligomers -- coriander essential oil -- lavender essential oil -- linalool -- neuroprotection; Materia medica, Vegetable -- Periodicals; Botany, Medical -- Periodicals; Medicinal plants -- Periodicals; Plant Extracts -- therapeutic use -- Periodicals; Plants, Medicinal -- Periodicals; 581.634
• DOI: 10.1002/ptr.6827
• Languages: English
• ISSNs: 0951-418X

Abstract

Abstract : Alzheimer's disease (AD) is a neurodegenerative disorder leading to cognitive deficits and cognitive decline. Since no cure or preventing therapy is currently available to counteract AD, natural‐derived compounds are investigated to find new potential neuroprotective agents for its treatment. In the present study, we tested the neuroprotective effect of lavender and coriander essential oils (EOs) and their main active constituent linalool, against the neurotoxicity elicited by Aβ1‐42 oligomers, a key molecular factor in the neurodegeneration of AD. Importantly, our findings on neuronally differentiated PC12 cells exposed to Aβ1‐42 oligomers are in accordance with previous in vivo studies reporting the neuroprotective potential of lavender and coriander EOs and linalool. We found that lavender and coriander EOs at the concentration of 10 μg/mL as well as linalool at the same concentration were able to improve viability and to reduce nuclear morphological abnormalities in cells treated with Aβ1‐42 oligomers for 24 hours. Lavender and coriander EOs and linalool also showed to counteract the increase of intracellular reactive oxygen species production and the activation of the pro‐apoptotic enzyme caspase‐3 induced by Aβ1‐42 oligomers. Our findings provide further evidence that these EOs and their main constituent linalool could be natural agents of therapeutic interest against Aβ1‐42 ‐induced neurotoxicity.