KMID : 1161420150180030273
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Journal of Medicinal Food 2015 Volume.18 No. 3 p.273 ~ p.279
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Genistein Alleviates ¥â-Amyloid-Induced Inflammatory Damage Through Regulating Toll-Like Receptor 4/Nuclear Factor ¥êB
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Ma Weiwei
Ding Bingjie Yu Huanling Yuan Linhong Xi Yuandi Xiao Rong
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Abstract
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Genistein (GEN), a major soybean isoflavone (SIF), might possess neuroprotective properties through its anti-inflammatory activity. We hypothesized that GEN could prevent the inflammatory damage detected in C6 cells induced by ¥â-amyloid peptides 25-35 (A¥â25-35). Accordingly, we evaluated the inflammatory damage induced by A¥â25-35 and the protective effect of GEN against A¥â25-35 in C6 cells. In our study, the C6 glial cells (rats glioma cell lines) were preincubated with or without GEN for 2?h following incubation with A¥â25-35 for another 24?h. Then, methylthiazolyl tetrazolium (MTT) assay was used to assess the cell viability. Immunofluorescence staining was used to identify the C6 cells. Inflammatory factors tumor necrosis factor (TNF)-¥á and interleukin (IL)-1¥â were analyzed by using enzyme-linked immunosorbent assay (ELISA). Western blot analysis and reverse transcription-polymerase chain reaction analysis were performed to assess the expression of Toll-like receptors 4 (TLR4), inhibitor of kappaB-alpha (I¥êB-¥á). The current results showed that GEN could alleviate A¥â25-35-induced cell apoptosis and prevent A¥â25-35-induced TNF-¥á and IL-1¥â release from C6 cells. In addition, GEN prevented A¥â25-35-induced upregulation of the gene and protein expression of TLR4, and GEN significantly upregulated the expression of I¥êB-¥á in C6 cells damaged by A¥â25-35. These results suggest that GEN can alleviate the inflammatory stress caused by A¥â25-35 treatment, which might be associated with the neuroprotective effect of GEN regulating the TLR4/NF¥êB signaling pathway.
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KEYWORD
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beta-amyloid peptides, genistein, inflammatory factors, neuroprotection
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