| 雷公藤次碱通过调控TLR4/MyD88/TRAF6信号通路抑制LPS诱导的RAW264.7细胞炎症反应 |
| 投稿时间：2021-11-16 修订日期：2022-09-07 点此下载全文 |
| 引用本文：汪滢,张敏新,林兵.雷公藤次碱通过调控TLR4/MyD88/TRAF6信号通路抑制LPS诱导的RAW264.7细胞炎症反应[J].药学实践杂志,2022,40(6):505~509 |
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| 基金项目:福建省自然科学基金资助项目（2017J05135） |
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| 中文摘要:目的 探讨雷公藤次碱抗炎活性及其作用机制。方法 用细胞计数盒-8 (CCK-8)法考察雷公藤次碱对小鼠单核巨噬细胞白血病细胞RAW 264.7 增殖活性的影响，用酶联免疫吸附法（ELISA）检测雷公藤次碱对脂多糖（LPS）诱导的RAW264.7细胞分泌细胞因子一氧化氮（NO）、白细胞介素-1β（IL-1β）、 肿瘤坏死因子α（TNF-α）和白细胞介素6（IL-6）的影响，用免疫印迹法考察雷公藤次碱对白介素受体相关激酶（IRAK）、肿瘤坏死因子受体相关蛋白6（TRAF6）、核因子κB抑制因子α（IκBα）、核因子κB（NF-κB p65）、分裂原激活的蛋白激酶p38（p38）、c-Jun氨基末端激酶（JNK）、细胞外调节蛋白激酶（ERK）在LPS刺激的RAW264.7细胞中的表达及其磷酸化的影响。结果 雷公藤次碱在25、50、100 μmol/L浓度下对RAW264.7细胞无显著毒性，并可显著抑制细胞因子NO、IL-1β、TNF-α和IL-6含量。免疫印迹法检测结果显示雷公藤次碱可显著抑制IRAK及TRAF6的表达；显著抑制ERK、P38和JNK的磷酸化；抑制IκBα的降解，降低NF-κB p65的核转运水平。结论 雷公藤次碱具有体外抗炎活性，其作用机制可能介导TLR4/MyD88/TRAF6信号通路。 |
| 中文关键词:雷公藤 雷公藤次碱 抗炎 toll样受体4 髓样分化因子88 核因子κB |
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| Wilforine inhibits LPS-induced inflammatory response in RAW264.7 cells by regulating the TLR4/MyD88/TRAF6 signaling pathway |
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| Abstract:Objective To investigate the anti-inflammatory effect and mechanism of wilforine. Methods Anti-inflammatory activity of wilforine was investigated in LPS-induced RAW264.7 cells. The cytokines production of RAW264.7 cells was analyzed by ELISA assay and the cell viability was assessed by CCK-8 method. The expression of TRAF6, the phosphorylation of IRAK, p38, ERK and JNK, the degradation of inhibitory κBα (IκBα) and the nuclear translocation of NF-κB p65 were further investigated by western blot. Results Triptolide had no significant toxicity to RAW264.7 cells at concentrations of 25, 50 and 100 μmol/L. and could significantly inhibit the contents of cytokines NO, IL-1β, TNF-α and IL-6. Wilforine significantly decreased the expression of TRAF6 and phosphorylation of IRAK, and inhibited the phosphorylation of ERK, p38, and JNK and degradation of IκBα, and reduced the level of nuclear translocation of NF-κB p65. Conclusion The anti-inflammatory activity of wilforine of LPS-induced RAW264.7 cells is probably via TLR4/MyD88/TRAF6 signaling pathway. |
| keywords:Tripterygium wilfordii wilforine anti-inflammation TLR4 MyD88 NF-κB |
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