Genistein Alleviates β-Amyloid-Induced Inflammatory Damage Through Regulating Toll-Like Receptor 4/Nuclear Factor κB
Genistein Alleviates β-Amyloid-Induced Inflammatory Damage Through Regulating Toll-Like Receptor 4/Nuclear Factor κB
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DOI：
10.1089/jmf.2014.3150
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发表时间：
2015-03-01
影响因子：
2.4
通讯作者：
Xiao, Rong
中科院分区：
文献类型：
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作者：
Ma, Weiwei;Ding, Bingjie;Xiao, Rong
染料木黄酮（GEN）是一种主要的大豆黄酮（SIF），可能通过其抗炎活性而具有神经保护作用。我们假设GEN可以预防由β-淀粉样肽25-35（A β 25-35）诱导的C6细胞中检测到的炎症损伤。因此，我们评估了A β 25-35诱导的炎症损伤和GEN对C6细胞中A β 25-35的保护作用。在我们的研究中，C6神经胶质细胞（大鼠神经胶质瘤细胞系）在与A β 25-35孵育另外24小时后，与或不与GEN预孵育2小时。MTT法检测细胞活力。免疫荧光染色鉴定C6细胞。采用酶联免疫吸附试验（ELISA）分析炎症因子肿瘤坏死因子（TNF）-α和白细胞介素（IL）-1 β。Western印迹分析和逆转录-聚合酶链反应分析，以评估Toll样受体4（TLR 4），抑制剂κ B-α（I κ B-α）的表达。目前的结果表明，GEN可以减轻A β 25-35诱导的细胞凋亡，并阻止A β 25-35诱导的C6细胞释放TNF-α和IL-1 β。此外，GEN阻止A β 25-35诱导的TLR 4基因和蛋白表达的上调，并且GEN显著上调A β 25-35损伤的C6细胞中I κ B-α的表达。提示GEN可减轻A β 25-35所致的炎症应激，其机制可能与GEN调节TLR 4/NF kappa B信号通路有关。
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 beta-amyloid peptides 25-35 (A beta 25-35). Accordingly, we evaluated the inflammatory damage induced by A beta 25-35 and the protective effect of GEN against A beta 25-35 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 beta 25-35 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)-alpha and interleukin (IL)-1 beta 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 kappa B-alpha). The current results showed that GEN could alleviate A beta 25-35-induced cell apoptosis and prevent A beta 25-35-induced TNF-alpha and IL-1 beta release from C6 cells. In addition, GEN prevented A beta 25-35-induced upregulation of the gene and protein expression of TLR4, and GEN significantly upregulated the expression of I kappa B-alpha in C6 cells damaged by A beta 25-35. These results suggest that GEN can alleviate the inflammatory stress caused by A beta 25-35 treatment, which might be associated with the neuroprotective effect of GEN regulating the TLR4/NF kappa B signaling pathway.