期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 418, 期 3, 页码 578-583出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2012.01.081
关键词
Inflammation; Astrocyte; Epicatechin; p65; TNF alpha; Flavonoids; Neurodegeneration
资金
- Medical Research Council
- Reading School of Pharmacy and the Department of Food and Nutritional Sciences
Neuroinflammation plays an important role in the progression of neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. Sustained activation of nuclear transcription factor kappa B (NF-kappa B) is thought to play an important role in the pathogenesis of neurodegenerative disorders. Flavonoids have been shown to possess antioxidant and anti-inflammatory properties and we investigated whether flavonoids, at submicromolar concentrations relevant to their bioavailability from the diet, were able to modulate NF-kappa B signalling in astrocytes. Using luciferase reporter assays, we found that tumour necrosis factor (TNF alpha, 150 ng/ml) increased NF-kappa B-mediated transcription in primary cultures of mouse cortical astrocytes, which was abolished on co-transfection of a dominant-negative I kappa B alpha construct. In addition, TNF alpha increased nuclear localisation of p65 as shown by immunocytochemistry. To investigate potential flavonoid modulation of NF-kappa B activity, astrocytes were treated with flavonoids from different classes; flavan-3-ols ((-)-epicatechin and (+)-catechin), flavones (luteolin and chrysin), a flavonol (kaempferol) or the flavanones (naringenin and hesperetin) at dietary-relevant concentrations (0.1-1 mu M) for 18 h. None of the flavonoids modulated constitutive or TNF alpha-induced NF-kappa B activity. Therefore, we conclude that NF-kappa B signalling in astrocytes is not a major target for flavonoids. (C) 2012 Elsevier Inc. All rights reserved.
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