Anti-inflammatory effects of daidzein on primary astroglial cell culture

• Published in: Nutritional neuroscience Vol. 12; no. 3; pp. 123 - 134
• Main Authors: Liu, Man-Hai, Lin, Yu-Shan, Sheu, Shiow-Yunn, Sun, Jui-Sheng
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 01.06.2009
• Subjects: Alzheimer Disease; AMYLOID BETA-PEPTIDE; Amyloid beta-Peptides - pharmacology; Animals; Anti-Inflammatory Agents - pharmacology; Astrocytes - cytology; Astrocytes - drug effects; Astrocytes - metabolism; Cell Division - drug effects; Cell Survival - drug effects; Cells, Cultured; Cytokines - genetics; DIADZEIN; Gene Expression - drug effects; Interleukin-1 - genetics; Interleukin-6 - genetics; Isoflavones - pharmacology; LIPOPOLYSACCHARIDE; Lipopolysaccharides - pharmacology; Mice; Mice, Inbred ICR; NEUROPROTECTIVE EFFECT; Nitric Oxide - biosynthesis; Receptors, Estrogen - genetics; RNA, Messenger - analysis; Tumor Necrosis Factor-alpha - genetics
• ISSN: 1028-415X; 1476-8305
• DOI: 10.1179/147683009X423274

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, 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-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 −12 M 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.