許秀蘊Liu MH; Lin YS; Sheu SY; Sun JS2026-05-212026-05-212009https://203.71.86.71/handle/123456789/22958INTRODUCTION: Alzheimer's disease is the common cause of dementia in old people. The pathological hallmarks of Alzheimer's disease include neuronal loss, deposition of amyloid-beta, and presence of neurofibrillary tangles. The endogenous steroid estrogen has been shown to affect neuronal growth, differentiation and survival, while isoflavones also have a neuroprotective effect on human cortical neurons. Daidzein, however, has a superior neuron-protective effect to other isoflavones. The present study is to determine whether daidzein is able to inhibit the production of pro-inflammatory mediators under amyloid-beta and lipopolysaccharide stimulation. MATERIALS AND METHODS: Astrocyte cells were stimulated with amyloid-beta or lipopolysaccharide in the absence and presence of diadzein. Nitric oxide released into the culture media was determined using the Griess reaction, and concentrations of IL-1, IL-6, TNF-alpha and estrogen receptor gene expression were measured by semi-quantitative real-time polymerase chain reaction assay. RESULTS: Diadzein-treatment increases astrocyte cell counts and attains its maximal effect at the 10(-12)M concentration. The addition of 20 microM amyloid-beta or 10(-6) g/ml LPS can significantly decrease the viability of astrocytes, up-regulated IL-1, IL-6, TNF-alpha mRNA and estrogen receptor expression; in addition, 1-h daidzein pre-treatment can restore the decreased viability of astrocytes induced by amyloid-beta or lipopolysaccharide as well as down-regulate their mRNA expression. CONCLUSIONS: It seems that this response is estrogen receptor-mediated. These results further increase the possibility that daidzein may have potential to ameliorate the inflammatory process and also alleviate the risk of Alzheimer's disease progression.en-US藥學系期刊論文article