Protective effects of Angelica sinensis extract on amyloid beta-peptide-induced neurotoxicity

作者：Huang Shih Hao; Lin Chun Mao; Chiang Been Huang^*

来源：Phytomedicine, 2008, 15(9): 710-721.

DOI：10.1016/j.phymed.2008.02.022

• Angelica sinensis
• beta-amyloid peptide
• glutathione
• mitochondria
• mitochondrial transmembrane potential (Delta Psi m)
• ROS

The protective effects of alcohol extract from the root of Angelica sinensis (AS) on beta-amylold peptide (A beta)-induced toxicity and the mechanism of these effects were investigated. A beta is a pathological hallmark of Alzheimer's disease; it decreased viability of Neuro 2A cells in a concentration-dependent manner with IC50 of 14.9 mu M. AS extract resulted in dose-dependent anti-A beta toxicity according to MTT assay. Reactive oxygen species (ROS) analysis revealed a significant production of hydrogen peroxide, decreased glutathione (GSH) levels and increased lipid peroxidation (TBARS value) in the A beta-treated Neuro 2A cells. The A beta-treated cells also showed a significant decline in the mitochondrial transmembrane potential (Delta Psi m) and increase in the mitochondrial volume, and portions of the cytoplasm were sequestered by a membrane-bound vacuole. The malfunctions of Neuro 2A cells caused by A beta were attenuated using AS extract. The AS extract protected cell viability against A beta-induced oxidative damage (ROS, TBARS, and GSH contents) and rescued the Delta Psi m levels in a dose-dependent manner: the dosages of 25, 50, 100, and 200 mu g/ml recovered 77%, 87%, 102%, and 105% of Delta Psi m, respectively. AS extract also recovered the enlarged mitochondria mass with dosages from 25 to 200 mu g/ml. The results of this study demonstrated that AS extract possessed the activity to prevent the neurotoxicity induced by A beta-associated oxidative stress, implying that AS has a potential role in the prevention of Alzheimer's diseases.

• 出版日期2008-9