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首页> 外文期刊>The American journal of Chinese medicine >Total Glycosides of Peony Protects Against Inflammatory Bowel Disease by Regulating IL-23/IL-17 Axis and Th17/Treg Balance
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Total Glycosides of Peony Protects Against Inflammatory Bowel Disease by Regulating IL-23/IL-17 Axis and Th17/Treg Balance

机译:牡丹的总糖苷通过调节IL-23 / IL-17轴和Th17 / Treg平衡来保护炎症肠疾病

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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.
机译:炎症性肠病(IBD)是一组自身免疫疾病,包括溃疡性结肠炎和克罗恩病,其特征在于肠道中的非特异性炎症。由于药理作用,牡丹(TGP)的​​总糖苷已被广泛用于治疗自身免疫性疾病。然而,TGP调节辅助17个细胞(TH17)/ T调节细胞(TREG)免疫平衡或白细胞介素23(IL-23)/ IL-17轴缺乏深度,以实现治疗IBD的目标。因此,本研究的目的是探讨TGP对实验性结肠炎小鼠的影响和相关机制。在本研究中,我们证明了TGP的给药有效衰减了TNBS诱导的结肠炎小鼠的结肠癌炎症,主要反映在显着改善的临床参数,降低炎症反应和髓过氧化物酶(MPO)活性,甚至更强的全身免疫能力和有效改善Th17 / treg免疫障碍。此外,在来自TGP处理的小鼠结肠的阳性分化4(CD4(+))饱和粒细胞的阳性簇中存在较强的免疫抑制能力,其特征在于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在IBD治疗中具有与水杨酰磺吡啶(SASP)类似的治疗效果。潜在机制可以至少部分地与调节Th17 / Treg细胞的不平衡和IL-23 / 1L-17-17炎性信号轴的抑制有关。

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