Department of Traditional Chinese Medicine, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Dingzhou Radi‑Glory Bio‑Chem Co., Ltd., Baoding, Hebei 073000, P.R. China.
Mol Med Rep. 2018 Mar;17(3):3455-3464. doi: 10.3892/mmr.2017.8321. Epub 2017 Dec 20.
The present study aimed to investigate the protective effects of magnolol on acute 2,4,6-trinitrobenzene sulfonic acid (TNBS)‑induced colitis, and its underlying mechanisms. Experimental colitis was induced by intracolonic administration of TNBS/ethanol into rats. The model rats were randomly assigned into groups: TNBS, magnolol (high, medium and low doses), and salazosulfapyridine (positive control). All intervention regimens were administered by oral gavage, once a day for 7 consecutive days, 24 h after colitis induction. Histological and biochemical changes in colonic inflammation were evaluated by hematoxylin and eosin and immunohistochemistry, respectively. Rats treated with all doses of magnolol exhibited decreased colonic myeloperoxidase activity (P<0.05 vs. TNBS), reduced serum levels of proinflammatory cytokines [including interleukin (IL)‑6 and IL‑17], and downregulated Toll‑like receptor-4 (TLR‑4) mRNA expression. Histological analysis revealed that medium and high doses of magnolol conferred an anti‑inflammatory effect, which was indicated by a decrease in disease activity index, an increase in thymus index, and downregulation of nuclear factor (NF)‑κB p65 mRNA and TLR‑4 protein expression. However, only high‑dose magnolol significantly ameliorated the elevated colon weight/length ratio. The results of the present study indicate that magnolol exerts protective effects against acute TNBS‑induced colitis in rats, and the TLR‑4/NF‑κB signaling pathway‑mediated inhibitory effect on inflammatory cascades may contribute to the protective activity of magnolol.
本研究旨在探讨厚朴酚对急性 2,4,6-三硝基苯磺酸(TNBS)诱导的结肠炎的保护作用及其机制。通过向大鼠结肠内给予 TNBS/乙醇来诱导实验性结肠炎。将模型大鼠随机分为以下几组:TNBS 组、厚朴酚(高、中、低剂量)组和柳氮磺胺吡啶(阳性对照)组。所有干预方案均通过口服灌胃给予,在结肠炎诱导后 24 小时开始,每天一次,连续 7 天。通过苏木精和伊红以及免疫组织化学分别评估结肠炎症的组织学和生化变化。用厚朴酚治疗的所有剂量组大鼠的结肠髓过氧化物酶活性降低(P<0.05 比 TNBS),促炎细胞因子[包括白细胞介素(IL)-6 和 IL-17]的血清水平降低,Toll 样受体-4(TLR-4)mRNA 表达下调。组织学分析表明,中剂量和高剂量的厚朴酚具有抗炎作用,这表现为疾病活动指数降低、胸腺指数增加、核因子(NF)-κB p65mRNA 和 TLR-4 蛋白表达下调。然而,只有高剂量的厚朴酚显著改善了升高的结肠重量/长度比。本研究结果表明,厚朴酚对大鼠急性 TNBS 诱导的结肠炎具有保护作用,TLR-4/NF-κB 信号通路对炎症级联反应的抑制作用可能是厚朴酚发挥保护作用的机制之一。