HUI-WEN LINYU-HSIANG KUAN2026-10-162026-10-162017-05-01Pure ID: 15335161Pure UUID: 1ea43d1d-91ca-4754-8d82-fa4e54ce1676https://www.scopus.com/pages/publications/85029808116https://scholars.csmu.edu.tw/handle/123456789/25178Yi-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 Aβ(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 Aβ(1-40)-induced death of primary cortical neurons. Primary cultures of Sprague-Dawley rat cortical neurons were exposed to Aβ(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 Aβ(1-40)-induced cytotoxicity and reversed Aβ(1-40)-induced β-Amyloid accumulation and acetylcholine receptor expression in a concentration-dependent manner. In addition, not only the Aβ(1-40)-reduced expression of N-methyl-D-Aspartate receptors 1/2A was reversed but also the Aβ(1-40)-induced reactive oxygen species generation and tau phosphorylation expression were inhibited by Yi-Chi-Tsung-Ming-Tang in a concentration-dependent manner.9enjournal article