首页> 美国卫生研究院文献>International Journal of Molecular Medicine >Soybean glyceollins mitigate inducible nitric oxide synthase and cyclooxygenase-2 expression levels via suppression of the NF-κB signaling pathway in RAW 264.7 cells
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Soybean glyceollins mitigate inducible nitric oxide synthase and cyclooxygenase-2 expression levels via suppression of the NF-κB signaling pathway in RAW 264.7 cells

机译:大豆糖蛋白通过抑制RAW 264.7细胞中的NF-κB信号传导途径来降低诱导型一氧化氮合酶和环氧合酶2的表达水平。

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摘要

Glyceollins, produced to induce disease resistance responses against specific species, such as an incompatible pathogen Phytophthora sojae in soybeans, have the potential to exhibit anti-inflammatory activity in RAW 264.7 cells. To investigate the anti-inflammatory effects of elicited glyceollins via a signaling pathway, we studied the glyceollin signaling pathway using several assays including RNA and protein expression levels. We found that soybean glyceollins significantly reduced LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production, as well as the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) via the suppression of NF-κB activation. Glyceollins also inhibited the phosphorylation of IκBα kinase (IKK), the degradation of IκBα, and the formation of NF-κB-DNA binding complex in a dose-dependent manner. Furthermore, they inhibited pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-18, but increased the generation of the anti-inflammatory cytokine IL-10. Collectively, the present data show that glyceollins elicit potential anti-inflammatory effects by suppressing the NF-κB signaling pathway in RAW 264.7 cells.
机译:产生的糖脂诱导针对特定物种(例如大豆中不相容的病原大豆疫霉)的抗病性反应,可能在RAW 264.7细胞中表现出抗炎活性。为了研究通过信号途径引起的糖蛋白的抗炎作用,我们使用包括RNA和蛋白质表达水平在内的几种测定方法研究了糖精蛋白信号传导途径。我们发现大豆糖蛋白可通过抑制NF-κB显着降低LPS诱导的一氧化氮(NO)和前列腺素E2(PGE2)的产生,以及诱导型NO合酶(iNOS)和环氧合酶2(COX-2)的表达。 κB激活。糖脂还以剂量依赖性方式抑制IκBα激酶(IKK)的磷酸化,IκBα的降解以及NF-κB-DNA结合复合物的形成。此外,它们抑制促炎细胞因子,例如肿瘤坏死因子(TNF)-α,白介素(IL)-1β和IL-18,但增加了抗炎细胞因子IL-10的产生。总体而言,本数据表明,糖蛋白通过抑制RAW 264.7细胞中的NF-κB信号传导途径引起潜在的抗炎作用。

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