Total Glycosides of Peony Protects Against Inflammatory Bowel Disease by Regulating IL-23/IL-17 Axis and Th17/Treg Balance
Total Glycosides of Peony Protects Against Inflammatory Bowel Disease by Regulating IL-23/IL-17 Axis and Th17/Treg Balance
复制标题
牡丹总苷通过调节 IL-23/IL-17 轴和 Th17/Treg 平衡预防炎症性肠病
DOI：
10.1142/s0192415x19500095
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发表时间：
2019-01-01
影响因子：
5.7
通讯作者：
Cao, Gang
中科院分区：
文献类型：
--
作者：
Li, Qinglin;Shan, Qiyuan;Cao, Gang
炎症性肠病（IBD）是一组自身免疫性疾病，包括溃疡性结肠炎和克罗恩病，其特征是肠道非特异性炎症。牡丹总苷（TGP）因其药理作用而被广泛用于治疗自身免疫性疾病。然而，TGP是否通过调节辅助性T细胞17细胞（Th17）/调节性T细胞（Treg）免疫平衡或白细胞介素23（IL-23）/IL-17轴来达到治疗IBD的目的尚缺乏深度。因此，本研究的目的是探讨TGP对实验性结肠炎小鼠的影响及其相关机制。在本研究中，我们证明TGP可有效减轻TNBS诱导的结肠炎小鼠的结肠炎症，主要体现在显着改善临床参数，降低炎症反应和髓过氧化物酶（MPO）活性，甚至增强全身免疫能力并有效改善Th17/Treg免疫紊乱。此外，来自TGP处理的小鼠结肠的分化4(CD4(+))阳性T淋巴细胞簇具有更强的免疫抑制能力，其特征是抑制高水平的炎症因子和增加的调节性T细胞。重要的是，高剂量TGP对IBD治疗具有与水杨磺胺吡啶（SASP）相似的治疗效果。其潜在机制可能至少部分与调节Th17/Treg细胞失衡和抑制IL-23/1L-17炎症信号轴有关。
Inflammatory bowel disease (IBD) is a group of autoimmune diseases, including ulcerative colitis and Crohn's disease, characterized by nonspecific inflammation in the gut. Total glycoside of peony (TGP) has been widely used for treatment of autoimmune diseases because of its pharmacological effects. However, it is lack of depth in whether TGP regulate T helper 17 cell (Th17) / T regulatory cell (Treg) immune balance or interleukin 23 (IL-23) / IL-17 axis to achieve the goal of treating IBD. Hence, the aim of this study was to investigate the effects of TGP on experimental colitis mice and the related mechanisms. In the present study, we demonstrated that administration of TGP effectively attenuates colonic inflammation of TNBS-induced colitis mice, mainly reflected in significantly improved clinical parameters, reduced inflammatory response and myeloperoxidase (MPO) activity, even stronger systemic immune ability and effective improvement of Th17/Treg immune disorders. In addition, there was a stronger immunosuppressive ability in a positive cluster of differentiation 4 (CD4(+)) Tlymphocytes from the TGP treated mouse colon, characterized by the inhibition of high levels of inflammatory factors and increased regulatory T cells. Importantly, high-dose TGP has similar therapeutic effects as salicylazosulfapyridine (SASP) on IBD treatment. The potential mechanisms might be, at least in part, related to the adjustment of imbalance of Th17/Treg cells and the inhibition of IL-23/1L-17 inflammatory signal axis.