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首页> 外文期刊>Phytotherapy research: PTR >Differential Inhibition of T Lymphocyte Proliferation and Cytokine Synthesis by [6]-Gingerol, [8]-Gingerol, and [10]-Gingerol
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Differential Inhibition of T Lymphocyte Proliferation and Cytokine Synthesis by [6]-Gingerol, [8]-Gingerol, and [10]-Gingerol

机译：[6]-姜汁，[8]-姜汁和[10]-姜汁对T淋巴细胞增殖和细胞因子合成的差异抑制

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[6]-Gingerol, [8]-gingerol, and [10]-gingerol are pungent components of fresh ginger, extracts of which inhibit various components of the inflammatory response. Because little is known regarding the effect of gingerols with different unbranched alkyl side chain lengths on the activation and effector function of T lymphocytes, we compared the effects of [6]-gingerol, [8]-gingerol, and [10]-gingerol on murine T lymphocyte proliferation, expression of CD25 and CD69 activation markers, cytokine synthesis, and interleukin (IL)-2 receptor signaling. All three gingerols inhibited DNA synthesis by T lymphocytes, as well as interferon-gamma synthesis. In contrast, only [8]-gingerol and [10]-gingerol inhibited CD25 and CD69 expression, and IL-2 synthesis. None of the gingerols affected IL-4 synthesis. Exogenous IL-2 enhanced T lymphocyte proliferation in the presence of [6]-gingerol but did not significantly increase T lymphocyte proliferation in the presence of [8]-gingerol or [10]-gingerol. In line with this finding, [8]-gingerol and [10]-gingerol impaired IL-2-induced proliferation of CTLL-2 cells, but constitutive CD25 expression was unaffected, indicating inhibition of IL-2 receptor signaling. In general, [10]-gingerol and [8]-gingerol were more potent inhibitors of T lymphocytes than [6]-gingerol. Suppression of T lymphocyte responses by gingerols suggests that these phytochemicals may be beneficial in chronic inflammatory conditions associated with excessive or inappropriate T lymphocyte activation. Copyright (C) 2015 John Wiley & Sons, Ltd.
机译：[6]-姜油，[8]-姜油和[10]-姜油是新鲜生姜的刺激性成分，其提取物抑制炎症反应的各种成分。由于对具有不同直链烷基侧链长度的生姜酚对T淋巴细胞的激活和效应功能的影响知之甚少，因此我们比较了[6]-姜油，[8]-姜油和[10]-姜油对T淋巴细胞的作用。小鼠T淋巴细胞增殖，CD25和CD69激活标记的表达，细胞因子合成以及白介素（IL）-2受体信号传导。所有三种姜醇均抑制T淋巴细胞的DNA合成以及干扰素-γ合成。相反，仅[8]-姜油酚和[10]-姜油酚抑制CD25和CD69表达以及IL-2合成。姜黄醇均不影响IL-4合成。在[6]-姜油醇存在下，外源IL-2增强了T淋巴细胞的增殖，但是在[8]-姜油醇或[10]-姜黄醇的存在下，外源IL-2并未显着增加T淋巴细胞的增殖。与该发现一致，[8]-姜油酚和[10]-姜油酚损害了IL-2诱导的CTLL-2细胞的增殖，但组成型CD25表达未受影响，表明IL-2受体信号转导受到抑制。通常，[10]-姜油酚和[8]-姜油酚是比[6]-姜油酚更有效的T淋巴细胞抑制剂。姜醇抑制T淋巴细胞反应表明这些植物化学物质在与过度或不适当的T淋巴细胞活化有关的慢性炎症中可能是有益的。版权所有（C）2015 John Wiley＆Sons，Ltd.

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