Nicotine attenuates β-amyloid peptide-induced neurotoxicity free radical and calcium accumulation in hippocampal neuronal cultures

摘要

class="enumerated" style="list-style-type:decimal">Recent studies indicate that neuronal loss in Alzheimer's disease (AD) is accompanied by the deposition of β-amyloid protein (Aβ) in senile plaques. Nicotine as a major component of cigarette smoke has been suggested to have a protective effect for neurons against Aβ neurotoxicity.Our present study demonstrates that nicotine protected cultured hippocampal neurons against the Aβ-induced apoptosis. Nicotine effectively inhibits apoptosis in hippocampal cultures caused by Aβ25–35 or Aβ1–40 treatment and increase of caspase activity induced by Aβ25–35 or Aβ1–40.Measurements of cellular oxidation and intracellular free Ca²⁺ showed that nicotine suppressed Aβ-induced accumulation of free radical and increase of intracellular free Ca²⁺.Cholinergic antagonist mecamylamine inhibited nicotine-induced protection against Aβ-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.