孙成宏, 赖新强, 张丽, 姚景春, 关永霞, 潘丽红, 徐真真, 闫莹. 牛蒡子苷元对炎性刺激剂PMA/ionomycin诱导淋巴细胞活化的抑制作用J. 药学学报, 2014,49(4): 482-489.
引用本文: 孙成宏, 赖新强, 张丽, 姚景春, 关永霞, 潘丽红, 徐真真, 闫莹. 牛蒡子苷元对炎性刺激剂PMA/ionomycin诱导淋巴细胞活化的抑制作用J. 药学学报, 2014,49(4): 482-489.
SUN Cheng-hong, LAI Xin-qiang, ZHANG Li, YAO Jing-chun, GUAN Yong-xia, PAN Li-hong, XU Zhen-zhen, YAN Ying. Inhibitory effect of arctigenin on lymphocyte activation stimulated with PMA/ionomycinJ. Acta Pharmaceutica Sinica, 2014,49(4): 482-489.
Citation: SUN Cheng-hong, LAI Xin-qiang, ZHANG Li, YAO Jing-chun, GUAN Yong-xia, PAN Li-hong, XU Zhen-zhen, YAN Ying. Inhibitory effect of arctigenin on lymphocyte activation stimulated with PMA/ionomycinJ. Acta Pharmaceutica Sinica, 2014,49(4): 482-489.

牛蒡子苷元对炎性刺激剂PMA/ionomycin诱导淋巴细胞活化的抑制作用

Inhibitory effect of arctigenin on lymphocyte activation stimulated with PMA/ionomycin

  • 摘要: 探讨牛蒡子苷元(arctigenin)对phorbol-12-myristate-13-acetate(PMA)/ionimycin(Ion)诱导的淋巴细胞活化、细胞因子表达、细胞增殖和细胞周期分布的影响。PMA/Ion处理小鼠淋巴结淋巴细胞,流式细胞术检测Arc对淋巴细胞CD69和CD25的表达、细胞因子的释放、细胞增殖以及细胞周期分布的影响。结果显示,浓度低于1.00 μmol·L-1时,Arc未表现出明显的细胞毒性,但可有效抑制PMA/Ion刺激的淋巴细胞CD69、CD25的表达和TNF-α、IFN-γ、IL-2、IL-4、IL-6、IL-10释放;同时,Arc显著抑制PMA/Ion活化的淋巴细胞增殖,并将细胞周期阻滞在G0/G1期。以上结果提示: 牛蒡子苷元可通过抑制淋巴细胞活化、细胞因子释放和细胞增殖发挥抗炎效应。

     

    Abstract: This study investigated the effect of arctigenin (Arc) on the cell activation, cytokines expression, proliferation, and cell-cycle distribution of mouse T lymphocytes. Mouse lymphocytes were prepared from lymph node and treated with Phorbol-12-myristate-13-acetate (PMA)/Ionimycin (Ion) and/or Arc. CD69, CD25, cytokines, proliferation and cell cycle were assayed by flow cytometry. The results showed that, at concentrations of less than 1.00 μmol·L-1, Arc expressed non-obvious cell damage to cultured lymphocytes, however, it could significantly down-regulate the expression of CD69 and CD25, as well as TNF-α, IFN-γ, IL-2, IL-4, IL-6 and IL-10 on PMA/Ion stimulated lymphocytes. At the same time, Arc could also inhibit the proliferation of PMA/Ion-activated lymphocytes and exhibited lymphocyte G0/G1 phase cycle arrest. These results suggest that Arc possesses significant anti-inflammatory effects that may be mediated through the regulation of cell activation, cytokines expression and cell proliferation.

     

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