Study on Protection Against β-Amyloid Peptide Toxicity With Oral Administration of Medicinal Herbs

Abstract

Seonghyangjeongkisan has been used as a therapeutic agent for cerebral disease in Korea, but its effectiveness in Alzheimer’s disease is not well known. In this study, we examined whether Seonghyangjeongkisan could protect against amyloid β–induced cytotoxicity in neuroblastoma cells and the brain. Seonghyangjeongkisan rescued amyloid β–induced cytotoxicity dose dependently and reduced amyloid β–induced apoptosis and reactive oxygen species. Injection of mice with amyloid β impaired performance on the passive avoidance task, but Seonghyangjeongkisan markedly improved memory impairment in mice, with it being more effective than tacrine treatment in mice. Moreover, the activation of stress-related kinases such as extracellular signal-regulated kinase, c-Jun NH2-terminal kinase, and p38 was suppressed, and the phosphorylation of τ protein, which is known as a marker of Alzheimer’s disease, was also suppressed by Seonghyangjeongkisan treatment in the hippocampus. These results demonstrate that Seonghyangjeongkisan reduces amyloid β-induced toxicity in the brain, suggesting that it may be a useful complementary therapy against Alzheimer’s disease.