Isoflavones inhibit poly(I:C)-induced serum, brain, and skin inflammatory mediators - relevance to chronic fatigue syndrome.

Isoflavones inhibit poly(I:C)-induced serum, brain, and skin inflammatory mediators - relevance to chronic fatigue syndrome.
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DOI:
10.1186/s12974-014-0168-5
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发表时间:
2014-10-31
影响因子:
9.3
通讯作者:
Theoharides TC
Theoharides TC
中科院分区:
医学1区
文献类型:
--
作者:
Vasiadi M;Newman J;Theoharides TC

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慢性疲劳综合征(CFS)是一种神经免疫内分泌疾病,影响约1%的美国人口,主要是女性。它的特点是在没有癌症或其他全身性疾病的情况下,持续6个月或更长时间的衰弱性疲劳。许多慢性疲劳综合症患者也有纤维肌痛和皮肤过敏,随着压力的加重而加重。促肾上腺皮质激素释放激素(CRH)和神经紧张素(NT)在应激下分泌,激活肥大细胞(MC),这是过敏反应所必需的,从而释放可能导致CFS症状的炎症介质。探讨异黄酮对多肌苷:多胞苷酸(poly(I:C))在有或无游泳应激下对小鼠运动活性和炎症介质表达以及人mcc激活的影响。雌性C57BL/6小鼠随机分为(a)对照组/不游泳组,(b)对照组/游泳组,(c)多肌苷组:多胞酸(聚(I: c))/不游泳组,(d)多肌苷组:多胞酸(聚(I: c))/游泳组。小鼠分别饲喂低或高异黄酮含量2周后,腹腔注射20 mg/kg poly(I:C),然后进行或不进行游泳应激15分钟。夜间监测运动活动,第二天处死动物。脑和皮肤的基因表达,以及血清水平,炎症介质被测量。数据分析采用非参数Mann-Whitney u检验。Poly(I:C)处理小鼠在24小时内运动活性降低,血清中TNF-α、IL-6、KC (IL-8/CXCL8小鼠同源物)、CCL2、3、4、5、CXCL10水平升高,脑组织和皮肤中TNF、IL-6、KC (Cxcl1、IL-8小鼠同源物)、CCL2、CCL4、CCL5和CXCL10基因表达升高。组氨酸脱羧酶(HDC)和NT的表达也有所增加,但仅在皮肤中。高异黄酮饮食逆转了这些影响。Poly(I:C)治疗降低小鼠运动活性,增加血清水平以及脑和皮肤炎症介质的基因表达。这些作用被异黄酮抑制,可能证明对慢性疲劳综合症有用。本文的在线版本(doi:10.1186/s12974-014-0168-5)包含补充材料,可供授权用户使用。
Chronic Fatigue Syndrome (CFS) is a neuroimmunoendocrine disease affecting about 1% of the US population, mostly women. It is characterized by debilitating fatigue for six or more months in the absence of cancer or other systemic diseases. Many CFS patients also have fibromyalgia and skin hypersensitivity that worsen with stress. Corticotropin-releasing hormone (CRH) and neurotensin (NT), secreted under stress, activate mast cells (MC) necessary for allergic reactions to release inflammatory mediators that could contribute to CFS symptoms. To investigate the effect of isoflavones on the action of polyinosinic:polycytidylic acid (poly(I:C)), with or without swim stress, on mouse locomotor activity and inflammatory mediator expression, as well as on human MC activation. Female C57BL/6 mice were randomly divided into four groups: (a) control/no-swim, (b) control/swim, (c) polyinosinic:polycytidylic acid (poly(I:C))/no swim, and (d) polyinosinic:polycytidylic acid (poly(I:C))/swim. Mice were provided with chow low or high in isoflavones for 2 weeks prior to ip injection with 20 mg/kg poly(I:C) followed or not by swim stress for 15 minutes. Locomotor activity was monitored overnight and animals were sacrificed the following day. Brain and skin gene expression, as well as serum levels, of inflammatory mediators were measured. Data were analyzed using the non-parametric Mann-Whitney U-test. Poly(I:C)-treated mice had decreased locomotor activity over 24 hours, and increased serum levels of TNF-α, IL-6, KC (IL-8/CXCL8 murine homolog), CCL2,3,4,5, CXCL10, as well as brain and skin gene expression of TNF, IL-6, KC (Cxcl1, IL8 murine homolog), CCL2, CCL4, CCL5 and CXCL10. Histidine decarboxylase (HDC) and NT expression were also increased, but only in the skin, over the same period. High isoflavone diet reversed these effects. Poly(I:C) treatment decreased mouse locomotor activity and increased serum levels and brain and skin gene expression of inflammatory mediators. These effects were inhibited by isoflavones that may prove useful in CFS. The online version of this article (doi:10.1186/s12974-014-0168-5) contains supplementary material, which is available to authorized users.
DOI: 10.1016/s0306-4522(96)00488-5
发表时间: 1997-04-01
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影响因子: 3.4
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