Icariin Inhibits Neurotoxicity Of Beta-Amyloid By Upregulating Cocaine-Regulated And Amphetamine-Regulated Transcripts

beta-amyloid peptide (A beta) is one of the main protein components of senile plaques contributing to Alzheimer's disease and it can induce neuronal apoptosis. In this study, it was found that icariin, a flavonoid extracted from Chinese Herba-Epimedii, inhibited A beta 42-induced neurotoxicity in a dose-dependent manner. The peak dose of icariin was 160 mu g/ml. In addition, mRNA and protein expressions of cocaine and amphetamine-regulated transcript (CART) were increased in A beta 42-treated neurons in the presence of 80 mu g/ml icariin. Moreover, CART-RNA interference was able to reverse neuroprotection of icariin on A beta 42. Furthermore, the expression of CART can be suppressed by extracellular signal-regulated kinase inhibitor instead of p38/JNK inhibitors, suggesting that icariin may be developed into therapeutic agents for Alzheimer's disease and other neurodegenerative diseases. NeuroReport 20:1564-1567 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.