Thymoquinone protects cultured rat primary neurons against amyloid β-induced neurotoxicity

Abstract

Thymoquinone (TQ) is the main constituent of the oil extracted from Nigella sativa seeds, which is known to be the active constituent responsible for many of the seed antioxidant and anti-inflammatory effects. The present study was designed to investigate whether TQ can protect against Alzheimer’s amyloid-β peptide (Aβ) induced neurotoxicity in rat primary neurons. Cultured hippocampal and cortical neurons were treated with Aβ1–42 and TQ simultaneously for 72h. Treatment with TQ efficiently attenuated Aβ1–42-induced neurotoxicity, as evidenced by improved cell viability. TQ also inhibited the mitochondrial membrane potential depolarization and reactive oxygen species generation caused by Aβ1–42. In addition, TQ restored synaptic vesicle recycling inhibition, partially reversed the loss of spontaneous firing activity, and inhibited Aβ1–42 aggregation in vitro. These beneficial effects may contribute to the protection against Aβ-induced neurotoxicity. In conclusion, our results suggested that TQ has neuroprotection potential against Aβ1–42 in rat hippocampal and cortical neurons and thus may be a promising candidate for Alzheimer disease treatment.