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Effect of polysaccharides from Vitis vinifera L. on NF-κB/IκB-α signal pathway and inflammatory factors in Alzheimer's model rats

机译:多糖从血管血管血糖L.对阿尔茨海默氏症模型大鼠NF-κB/IκB-α信号途径和炎症因子的影响

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The aim of this study was to investigate the mechanism of action underlying the effect of polysaccharide from Vitis vinifera L. (VTP) on the nuclear factor kappa B/inhibitor kappa B alpha (NF-κB/IκB-α) signaling pathway and related inflammatory factors in hippocampus of rats with Alzheimer's disease (AD). Amyloid-β 25–35 was injected into the hippocampus to establish AD model rats, and the rats were administered with donepezil and VTP. The levels of interleukin-1β, interleukin-6 and tumour necrosis factor-α in the serum were determined by enzyme-linked immunosorbent assay. The phosphorylation level, protein and gene expression of NF-κBp65 and IκB-α in hippocampus were detected by immunohistochemistry, western blot and real-time quantitative polymerase chain reaction (PCR), respectively. VTP effectively improved the learning and memory ability of AD rats. Transmission electron microscopy indicated that VTP reduced the toxic effects of amyloid-β 25–35 on neurons in AD rats. Enzyme-linked immunosorbent assay showed that VTP inhibited the expression of interleukin-1β, interleukin-6 and tumour necrosis factor-α in a dose-dependent manner. Compared with the model group, the expression levels of NF-κBp65 in the nucleus of the VTP group decreased, which was consistent with the Western blotting results. The expression of p-IκB-α and IκB-α, and, the mRNA level of NF-κBp65 and IκB-α in VTP group were significantly decreased compared to that in the model group, indicating that VTP has a therapeutic effect on AD. Its mechanism may be related to the inhibition of inflammatory response.
机译:本研究的目的是调查多糖从肺血管癌患者的作用机制对核因子Kappa B /抑制剂KappaBα(NF-κB/IκB-α)信号传导途径和相关炎症阿尔茨海默病(AD)大鼠海马的因素。将淀粉样蛋白-β25-35注入海马以建立广告模型大鼠,并且大鼠用多胺和VTP施用。血清中白细胞介素-1β,白细胞介素-6和肿瘤坏死因子-α的水平通过酶联免疫吸附测定法测定。通过免疫组织化学,Western印迹和实时定量聚合酶链反应(PCR)检测Hippocampus中NF-κBP65和IκB-α的磷酸化水平,蛋白质和基因表达。 VTP有效提高了广告大鼠的学习和记忆能力。透射电子显微镜表明VTP降低了Ad大鼠神经元对神经元的毒性作用。酶联免疫吸附试验显示VTP以剂量依赖性方式抑制白细胞介素-1β,白细胞介素-6和肿瘤坏死因子-α的表达。与模型组相比,VTP组核中NF-κBP65的表达水平降低,这与蛋白质印迹结果一致。与模型组相比,VTP组NF-κBP65和VTP组中NF-κBP65和IκB-α的mRNA水平的表达显着降低,表明VTP对AD具有治疗效果。其机制可能与抑制炎症反应有关。

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