The Immunoregulatory Effects of Traditional Chinese Medicine on Psoriasis via its Action on Interleukin: Advances and Considerations.

The Immunoregulatory Effects of Traditional Chinese Medicine on Psoriasis via its Action on Interleukin: Advances and Considerations.
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DOI:
10.1142/s0192415x18500386
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发表时间:
2018-06
期刊:
The American journal of Chinese medicine
影响因子:
--
通讯作者:
Min-feng Wu;Yu Deng;Su-na Li;Yu Chen;Dongjie Guo;Xing-xiu Jin;Qi Xu;Bin Li;Fulun Li
Min-feng Wu;Yu Deng;Su-na Li;Yu Chen;Dongjie Guo;Xing-xiu Jin;Qi Xu;Bin Li;Fulun Li
中科院分区:
其他
文献类型:
--
作者:
Min-feng Wu;Yu Deng;Su-na Li;Yu Chen;Dongjie Guo;Xing-xiu Jin;Qi Xu;Bin Li;Fulun Li

文献摘要

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银屑病是一种以红斑和白色鳞屑为特征的慢性炎症性皮肤病。银屑病的发病机制尚不清楚。虽然西医采用激素疗法和物理疗法相结合的方法,但停药后往往会复发。传统中药(TCM)具有治疗特点,通过调节不平衡的免疫系统,如靶向白细胞介素,可能是临床有效的配方。本文就近年来中医药通过白细胞介素调节银屑病免疫功能的研究进展进行综述,并对相关机制进行系统总结。导致银屑病的常见途径有三种:(1)Th 17细胞分泌IL-17,受IL-23刺激;(2)Th 1细胞在Th 17细胞的帮助下分泌IL-21、TNF-[式:见正文]和IFN-[式:见正文];(3)Th 22细胞在Th 17细胞的刺激下分泌IL-22。临床和实验研究表明,中药可能通过拮抗或调节IL-23/IL-17轴,抑制主要通路,从而达到治疗银屑病的目的。
Psoriasis is a chronic inflammatory cutaneous disease characterized by clinical manifestations of erythema and white scales. The pathogenesis of psoriasis is not yet clear. Despite a combination of hormonal therapy and physiotherapy used in Western medicine, the condition often relapses after withdrawal of drugs. Traditional Chinese medicine (TCM) has therapeutic features and may be a clinically effective formula by regulating unbalanced immune systems, such as by targeting interleukins. In this paper, we review recent research about how Chinese medicine immunoregulates psoriasis via interleukins, and systematically summarizes the related mechanisms. There are three common pathways leading to psoriasis: (1) Th17 cells secrete IL-17, which is stimulated by IL-23; (2) Th1 cells secrete IL-21, TNF-[Formula: see text] and IFN-[Formula: see text], with the help of Th17 cells; (3) Th22 cells secrete IL-22 under the stimulation of Th17 cells. Clinical and experiment data indicate that TCM could modify psoriasis by antagonizing or regulating interleukin and IL-23/IL-17 axis to inhibit the main pathways.