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Nicotine attenuates β ‐amyloid peptide‐induced neurotoxicity, free radical and calcium accumulation in hippocampal neuronal cultures
Author(s) -
Liu Qiang,
Zhao Baolu
Publication year - 2004
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0705653
Subject(s) - neurotoxicity , mecamylamine , nicotine , chemistry , hippocampal formation , calcium in biology , cholinergic , pharmacology , senile plaques , intracellular , nicotinic agonist , receptor , microbiology and biotechnology , neuroscience , alzheimer's disease , medicine , biology , biochemistry , toxicity , organic chemistry , disease
Recent studies indicate that neuronal loss in Alzheimer's disease (AD) is accompanied by the deposition of β ‐amyloid protein (A β ) in senile plaques. Nicotine as a major component of cigarette smoke has been suggested to have a protective effect for neurons against A β neurotoxicity. Our present study demonstrates that nicotine protected cultured hippocampal neurons against the A β ‐induced apoptosis. Nicotine effectively inhibits apoptosis in hippocampal cultures caused by A β 25–35 or A β 1–40 treatment and increase of caspase activity induced by A β 25–35 or A β 1–40 . Measurements of cellular oxidation and intracellular free Ca 2+ showed that nicotine suppressed A β ‐induced accumulation of free radical and increase of intracellular free Ca 2+ . Cholinergic antagonist mecamylamine inhibited nicotine‐induced protection against A β ‐induced caspase‐3 activation and ROS accumulation. The data show that the protection of nicotine is partly via nicotinic receptors. Our results suggest that nicotine may be beneficial in retarding the neurodegenerative diseases such as AD.British Journal of Pharmacology (2004) 141 , 746–754. doi: 10.1038/sj.bjp.0705653