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β淀粉样肽(25-35)通过 Toll 样受体引发炎症,染料木黄酮在 BV-2 细胞中的抗炎作用。

Beta amyloid peptide (25-35) leading to inflammation through Toll-like receptors and the anti-inflammatory effect of genistein in BV-2 cells.

机构信息

School of Public Health, Capital Medical University, No.10 Xitoutiao, You An Men, Beijing, People's Republic of China,

出版信息

J Mol Neurosci. 2013 Nov;51(3):771-8. doi: 10.1007/s12031-013-0063-z. Epub 2013 Aug 15.

Abstract

Genistein, the main soy isoflavone component, has received much attention for its potential multifunction. Here, we reported that in BV-2 cells, genistein significantly inhibited beta amyloid peptides 25-35 (Aβ25-35)-induced inflammatory response. The results indicated that Aβ25-35-stimulated BV-2 cells upregulated Toll-like receptors 2 and 4, Myd88, and IKK gene expression with the increasing expression of IL-6 and decreasing expression of TGF-β and IL-10. Further, inhibiting TLR4 expression with small interfering RNA prevented the inflammatory response induced by Aβ25-35, indicating the key role of TLRs in Aβ-mediated inflammation. Genistein pre-treated BV-2 cells showed less inflammatory response when exposed to Aβ25-35. These results suggested that Aβ induced BV-2 cells inflammation though TLRs and genistein has an anti-inflammatory effect in vitro.

摘要

染料木黄酮是大豆异黄酮的主要成分,因其潜在的多功能性而备受关注。在这里,我们报道在 BV-2 细胞中,染料木黄酮可显著抑制β淀粉样肽 25-35(Aβ25-35)诱导的炎症反应。结果表明,Aβ25-35 刺激 BV-2 细胞上调 Toll 样受体 2 和 4、Myd88 和 IKK 基因表达,同时 IL-6 表达增加,TGF-β和 IL-10 表达减少。此外,用小干扰 RNA 抑制 TLR4 表达可阻止 Aβ25-35 诱导的炎症反应,表明 TLRs 在 Aβ 介导的炎症中起关键作用。当用 Aβ25-35 处理预先用染料木黄酮处理的 BV-2 细胞时,炎症反应较少。这些结果表明,Aβ 通过 TLRs 诱导 BV-2 细胞炎症,而染料木黄酮在体外具有抗炎作用。

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