Anti-inflammatory effects of daidzein on primary astroglial cell culture

Man Hai Liu, Yu Shan Lin, Shiow Yunn Sheu, Jui Sheng Sun

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29 引文 斯高帕斯(Scopus)


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-β, andInstitute of 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-β and lipopolysaccharide stimulation. Materials and methods: Astrocyte cells were stimulated with amyloid-β 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-α 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 -12M concentration. The addition of 20 μM amyloid-β or 10 -6 g/ml LPS can significantly decrease the viability of astrocytes, up-regulated IL-1, IL-6, TNF-α mRNA and estrogen receptor expression; in addition, 1-h daidzein pre-treatment can restore the decreased viability of astrocytes induced by amyloid-β 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.

頁(從 - 到)123-134
期刊Nutritional Neuroscience
出版狀態已發佈 - 6月 1 2009

ASJC Scopus subject areas

  • 醫藥(雜項)
  • 營養與營養學
  • 神經科學 (全部)


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