Study on protection against b-amyloid peptide toxicity with oral administration of medicinal herbs

Seonghyangjeongkisan has been used as a therapeutic agent for cerebral disease in Korea, but its effectiveness in Alzheimer'sdisease is not well known. In this study, we examined whether Seonghyangjeongkisan could protect against amyloid b'inducedcytotoxicity in neuroblastoma cells and the brain. Seonghyangjeongkisan rescued amyloid b'induced cytotoxicity dose dependentlyand reduced amyloid b'induced apoptosis and reactive oxygen species. Injection of mice with amyloid b impaired performanceon the passive avoidance task, but Seonghyangjeongkisan markedly improved memory impairment in mice, with it beingmore effective than tacrine treatment in mice. Moreover, the activation of stress-related kinases such as extracellular signalregulatedkinase, c-Jun NH2-terminal kinase, and p38 was suppressed, and the phosphorylation of t protein, which is knownas a marker of Alzheimer's disease, was also suppressed by Seonghyangjeongkisan treatment in the hippocampus. These resultsdemonstrate that Seonghyangjeongkisan reduces amyloid b-induced toxicity in the brain, suggesting that it may be a useful complementarytherapy against Alzheimer's disease.