Yi-Chi-Tsung-Ming-Tang Reduced A beta(1-40)-induced Neurotoxicity via of Acetylcholine and NMDA Receptors Expression, ROS Generation and Tau Phosphorylation

摘要

Yi-Chi-Tsung-Ming-Tang is a traditional Chinese medicine formula often prescribed for preventing or treating dizziness, tinnitus, mental fatigue and blurred vision. Recent study has demonstrated that A beta(1-40)-induced neurotoxicity could be improved by this drug. The aim of present study was to determine the effects and protective mechanism of Yi-Chi-Tsung-Ming-Tang on A beta(1-40)-induced death of primary cortical neurons. Primary cultures of Sprague-Dawley rat cortical neurons were exposed to A beta(1-40), after the treatment with Yi-Chi-Tsung-Ming-Tang for 1 h. Methyl-thiazolyl-tetrazolium reduction assays were used to detect cell viability and the expression of acetylcholine receptors, N-methyl-D-aspartate receptors and phosphorylated and non-phosphorylated forms of tau were measured by western blot. Fluorometric assays were applied to detect the generation of reactive oxygen species. Pretreatment of primary cortical neurons with Yi-Chi-Tsung-Ming-Tang significantly inhibited A beta(1-40)-induced cytotoxicity and reversed A beta(1-40)-induced beta-amyloid accumulation and acetylcholine receptor expression in a concentration-dependent manner. In addition, not only the A beta(1-40)-reduced expression of N-methyl-D-aspartate receptors 1/2A was reversed but also the A beta(1-40)-induced reactive oxygen species generation and tau phosphorylation expression were inhibited by Yi-Chi-Tsung-Ming-Tang in a concentration-dependent manner.