Incensole acetate prevents beta-amyloid-induced neurotoxicity in human olfactory bulb neural stem cells

Publication date: September 2018Source: Biomedicine & Pharmacotherapy, Volume 105Author(s): Mohammed A. El-Magd, Sara F. Khalifa, Faisal Abdulrahman A. Alzahrani, Abdelnaser A. Badawy, Eman S. El-Shetry, Lamess M. Dawood, Mohammed M. Alruwaili, Hedib A. Alrawaili, Engi F. Risha, Fathy M. El-Taweel, Hany E. MareiAbstractβ-Amyloid peptide (Aβ) is a potent neurotoxic protein associated with Alzheimer’s disease (AD) which causes oxidative damage to neurons. Incensole acetate (IA) is a major constituent of Boswellia carterii resin, which has anti-inflammatory and protective properties against damage of a large verity of neural subtypes. However, this neuroprotective effect was not studied on human olfactory bulb neural stem cells (hOBNSCs). Herein, we evaluated this effect and studied the underlying mechanisms. Exposure to Aβ25–35 (5 and 10 μM for 24 h) inhibited proliferation (revealed by downregulation of Nestin and Sox2 gene expression), and induced differentiation (marked by increased expression of the immature neuronal marker Map2 and the astrocyte marker Gfap) of hOBNSCs. However, pre-treatment with IA (100 μM for 4 h) stimulated proliferation and differentiation of neuronal, rather than astrocyte, markers. Moreover, IA pretreatment significantly decreased the Aβ25–35-induced viability loss, apoptotic rate (revealed by decreased caspase 3 activity and protein expression, downregulated expression of Bax, caspase 8, cyto c, caspase3, and upregulated express...
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research