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首页> 外文期刊>Biochemical Pharmacology >Oral flavonoids delay recovery from experimental autoimmune encephalomyelitis in SJL mice.
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Oral flavonoids delay recovery from experimental autoimmune encephalomyelitis in SJL mice.

机译：口服类黄酮延缓了SJL小鼠实验性自身免疫性脑脊髓炎的恢复。

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Flavonoids are food components that appear to have potential beneficial health effects. There is a range of in vitro studies supporting the anti-oxidant and anti-inflammatory properties of flavonoids. Previously, we demonstrated that in vitro flavonoids, including luteolin and apigenin, inhibit proliferation and IFN-gamma production by murine and human autoimmune T cells. In the present study, we examined the effects of oral flavonoids as well as of curcumin on autoimmune T cell reactivity in mice and on the course of experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. Continuous oral administration of flavonoids significantly affected antigen-specific proliferation and IFN-gamma production by lymph node-derived T cells following immunization with an EAE-inducing peptide. Both luteolin and apigenin suppress proliferative responses as they did in vitro, whereas IFN-gamma production on the other hand was enhanced. Other flavonoids exerted differential effects on proliferationand IFN-gamma production. The effects of flavonoids and curcumin on EAE were assessed using either passive transfer of autoimmune T cells or active disease induction. In passive EAE, flavonoids led to delayed recovery of clinical symptoms rather than to any reduction in disease. In active EAE, the effects were less pronounced but also, in this case, the flavonoid hesperitin delayed recovery. Oral curcumin had overall mild but beneficial effects. Our results indicate that oral flavonoids fail to beneficially influence the course of EAE in mice but, instead, suppress recovery from acute inflammatory damage.
机译：类黄酮是食品成分，似乎对健康具有潜在的有益影响。有大量的体外研究支持类黄酮的抗氧化和抗炎特性。之前，我们证明了体外黄酮类化合物（包括木犀草素和芹菜素）可抑制鼠类和人类自身免疫性T细胞的增殖和IFN-γ的产生。在本研究中，我们检查了口服类黄酮以及姜黄素对小鼠自身免疫性T细胞反应性以及实验性自身免疫性脑脊髓炎（EAE）（一种多发性硬化症模型）的作用。在用EAE诱导肽免疫后，连续口服黄酮类药物显着影响了淋巴结来源的T细胞的抗原特异性增殖和IFN-γ的产生。木犀草素和芹菜素都可以抑制增殖反应，就像在体外一样，而IFN-γ的产生却可以增强。其他类黄酮对增殖和IFN-γ产生有不同的作用。使用自身免疫性T细胞的被动转移或主动性疾病诱导评估了类黄酮和姜黄素对EAE的影响。在被动EAE中，类黄酮导致临床症状的恢复延迟，而不是疾病的减少。在活跃的EAE中，这种作用不太明显，但是在这种情况下，类黄酮橙皮素延迟了恢复。口服姜黄素总体上具有轻微但有益的作用。我们的结果表明，口服黄酮类化合物不能有益地影响小鼠EAE的病程，但会抑制急性炎症损害的恢复。

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