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Cell J. 2017;18(4):556-564. doi: 10.22074/cellj.2016.4722. Epub 2016 Sep 26.

[No title available]

Cell journal

Maliheh Soodi, Abolfazl Dashti, Homa Hajimehdipoor, Shole Akbari, Nasim Ataei

Affiliations

  1. Department of Toxicology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
  2. Department of Traditional Pharmacy, School of Traditional Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

PMID: 28042540 PMCID: PMC5086334 DOI: 10.22074/cellj.2016.4722

Abstract

OBJECTIVE: Extracellular deposition of the beta-amyloid (Aβ) peptide, which is the main finding in the pathophysiology of Alzheimer's disease (AD), leads to oxidative damage and apoptosis in neurons.

MATERIALS AND METHODS: This study was an

RESULTS: The acidic fraction could protect CGNs from Aβ-induced cytotoxicity. Mecamylamine did not abolish the protective effect of the acidic fraction. AChE activity, ROS production, lipid peroxidation, and caspase-3 activity increased after Aβ incubation. Preincubation with the acidic fraction of

CONCLUSION: Our results indicated that the protective effect of the acidic fraction of M. officinalis was not mediated through nicotinic receptors. This fraction could protect CGNs through antioxidant and anti-apoptotic activities.

Keywords: Alzheimer’s Disease; Apoptosis; Melissa officinalis; Nicotinic Receptor

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