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Thymoquinone protects cultured rat primary neurons against amyloid ß-induced neurotoxicity.
Alhebshi, A H; Gotoh, M; Suzuki, I.
Affiliation
  • Alhebshi AH; Department of Biotechnology, Graduate School of Bionics, Tokyo University of Technology, 1404-1Katakura, Hachioji, Tokyo 192-0982, Japan.
Biochem Biophys Res Commun ; 433(4): 362-7, 2013 Apr 19.
Article in En | MEDLINE | ID: mdl-23537659
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-ß peptide (Aß) induced neurotoxicity in rat primary neurons. Cultured hippocampal and cortical neurons were treated with Aß1-42 and TQ simultaneously for 72 h. Treatment with TQ efficiently attenuated Aß1-42-induced neurotoxicity, as evidenced by improved cell viability. TQ also inhibited the mitochondrial membrane potential depolarization and reactive oxygen species generation caused by Aß1-42. In addition, TQ restored synaptic vesicle recycling inhibition, partially reversed the loss of spontaneous firing activity, and inhibited Aß1-42 aggregation in vitro. These beneficial effects may contribute to the protection against Aß-induced neurotoxicity. In conclusion, our results suggested that TQ has neuroprotection potential against Aß1-42 in rat hippocampal and cortical neurons and thus may be a promising candidate for Alzheimer disease treatment.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Peptide Fragments / Amyloid beta-Peptides / Benzoquinones / Cytoprotection / Neurons Limits: Animals Language: En Journal: Biochem Biophys Res Commun Year: 2013 Document type: Article Affiliation country: Japan Country of publication: United States

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Peptide Fragments / Amyloid beta-Peptides / Benzoquinones / Cytoprotection / Neurons Limits: Animals Language: En Journal: Biochem Biophys Res Commun Year: 2013 Document type: Article Affiliation country: Japan Country of publication: United States