Department of Gastroenterology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325035, P.R. China.
Department of Clinical Medicine, Renji College of Wenzhou Medical University, Wenzhou, Zhejiang 325035, P.R. China.
Mol Med Rep. 2017 Dec;16(6):8265-8276. doi: 10.3892/mmr.2017.7598. Epub 2017 Sep 25.
The imbalance between effector CD4+ T helper 17 (Th17) and regulatory CD4+ T cells (Treg) cells and their associated cytokines, have been associated with the pathogenesis of inflammatory bowel disease (IBD). Total glycosides of paeony (TGP) is an alternative immunomodulatory agent that is widely used for the treatment of autoimmune diseases. The present study aimed to evaluate the modulatory effect of TGP in a rat model of colitis induced by 2,4,6‑trinitrobenzene sulfonic acid (TNBS). TGP was administered intragastrically 24 h after the TNBS intrarectal instillation for 7 days. TGP treatment ameliorated the clinical status and reversed the histopathologic severity of acute TNBS colitis. Furthermore, TGP inhibited the levels of Th17‑associated cytokines interleukin (IL)‑17, IL‑6, tumor necrosis factor‑α, whereas the expression levels of Treg‑associated cytokines IL‑10, transforming growth factor‑β in the plasma, colon, spleen and mesenteric lymph nodes (MLN). Additionally, TGP reduced the percentage of Th17 cells; however, the proportion of Treg cells in the spleen and MLN was increased. The present study also observed a suppression of Th17‑associated transcription factor, termed retinoid‑related orphan receptor‑γt (ROR‑γt). However, expression of the Treg‑associated transcription factor forkhead boxp3 was increased in the TGP treatment group. Therefore, the present findings suggest that TGP has a regulatory role in modulating the balance of Th17 and Treg cells to ameliorate the TNBS‑induced colitis and support the strategy of using TGP to treat IBD.
白芍总苷通过调节辅助性 T 细胞 17（Th17）与调节性 T 细胞（Treg）及其相关细胞因子的失衡，可参与炎症性肠病（IBD）的发病机制。白芍总苷（TGP）是一种免疫调节药物，广泛用于治疗自身免疫性疾病。本研究旨在评估 TGP 对 2,4,6-三硝基苯磺酸（TNBS）诱导的结肠炎大鼠模型的调节作用。TNBS 直肠内灌注后 24 h 给予 TGP 灌胃，连续给药 7 d。TGP 治疗可改善急性 TNBS 结肠炎的临床状态并逆转组织病理学严重程度。此外，TGP 抑制 Th17 相关细胞因子白细胞介素（IL）-17、IL-6、肿瘤坏死因子-α的水平，同时抑制血浆、结肠、脾和肠系膜淋巴结（MLN）中 Treg 相关细胞因子 IL-10、转化生长因子-β的表达水平。此外，TGP 降低 Th17 细胞的比例；然而，脾和 MLN 中 Treg 细胞的比例增加。本研究还观察到 Th17 相关转录因子维甲酸相关孤儿受体-γt（ROR-γt）的表达受到抑制。然而，TGP 治疗组 Treg 相关转录因子叉头框蛋白 3 的表达增加。因此，本研究结果表明，TGP 具有调节 Th17 和 Treg 细胞平衡的作用，可改善 TNBS 诱导的结肠炎，并支持使用 TGP 治疗 IBD 的策略。
