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    題名: Anti-inflammatory effects of daidzein on the primary astroglial cells culture
    作者: 許秀蘊
    Liu MH;Lin YS;Sheu SY;Sun JS
    貢獻者: 藥學系
    日期: 2009
    上傳時間: 2009-08-17 09:55:33 (UTC+8)
    摘要: INTRODUCTION: 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.
    關聯: Nutritional Neuroscience.(12):123-134.
    資料類型: article
    顯示於類別:[藥學系] 期刊論文

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