The protective effects of tanshinone IIA on β-amyloid protein (1–42)-induced cytotoxicity via activation of the Bcl-xL pathway in neuron

• Published in: Brain research bulletin Vol. 88; no. 4; pp. 354 - 358
• Main Authors: Qian, Yi-Hua, Xiao, Qingli, Xu, Jan
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.07.2012
• Subjects: Alzheimer's disease; Amyloid beta-Peptides - toxicity; Animals; Apoptosis; Apoptosis - drug effects; Apoptosis - physiology; Axons; Bcl-x protein; bcl-X Protein - metabolism; Bcl-xL/Bcl-xS; beta -Amyloid; Blotting, Western; Brain; Cell survival; Cortex; Cytotoxicity; Diterpenes, Abietane - pharmacology; Herbal medicines; Mice; mRNA; Neurodegenerative diseases; Neurology; Neuron; Neurons; Neurons - drug effects; Neurons - metabolism; Neuroprotection; Neuroprotective Agents - pharmacology; Peptide Fragments - toxicity; Reverse Transcriptase Polymerase Chain Reaction; Tanshinone IIA; tanshinones; β-amyloid protein; β-amyloid protein; Tanshinone IIA; Neuron; Bcl-xL/Bcl-xS; Alzheimer's disease
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/j.brainresbull.2012.03.007

Highlights ► Tanshinone IIA (tanIIA) is one of ingredients of tanshinone which is lipophilic. ► Apoptosis is a crucial pathway in neuronal loss in Alzheimer's disease (AD). ► Deposition of β-amyloid protein(Aβ) within brain is the pathologic hallmarks of AD. ► We explore the protective effects of tanIIA on Aβ1–42 -induced cytotoxicity. ► TanIIA protected neurons against toxicity of Aβ via activation of the Bcl-xL pathway.