Pu Zhichen, Han Chengzheng, Zhang Weiwei, Xu Maodi, Wu Zijing, Liu Yanhao, Wu Min, Sun Hui, Xie Haitang
Anhui Provincial Center for Drug Clinical Evaluation, Yijishan Hospital of Wannan Medical College Wuhu 241001, Anhui, China.
Clinic of Integrated Traditional Chinese and Western Medicine, Yijishan Hospital of Wannan Medical College Wuhu 241001, Anhui, China.
Am J Transl Res. 2019 Jul 15;11(7):3992-4009. eCollection 2019.
Arctigenin (ARC-G) is the main active ingredient extracted from Great Burdock Achene, with extensive pharmacological effects. In addition, ARC-G has been suggested to show excellent efficacy on inflammatory disease. This study aimed to defined that the function of Arctigenin attenuates inflammation in dextran sulfate sodium (DSS)-induced acute colitis, to determine its possible mechanism. Mice was induced by giving 2.0% DSS in the drinking water for DSS-induced acute colitis. Mice of acute colitis were injected intraperitoneally with 20 mg/kg per day of Arctigenin for 7 days. MPO activity levels were measured using MPO activity kits. Western Blot Analysis was used to determine the protein expression. Arctigenin prevents colitis and attenuates inflammation in DSS-induced acute colitis. Arctigenin suppressed NLRP3 inflammasome by SIRT1 in DSS-induced acute colitis. In THP-1 cell by LPS model, Arctigenin suppressed NLRP3, caspase-1 and IL-1β protein expression by SIRT1. Si-NLRP3 increases the effects of Arctigenin on inflammation in THP-1 cell by LPS model. Si-SIRT1 decreases the effects of Arctigenin on inflammation in THP-1 cell by LPS model. INF39, NLRP3 inhibitor also increased the effects of Arctigenin on inflammation in DSS-induced acute colitis. SIRT1 inhibitor also decreases the effects of Arctigenin on inflammation in DSS-induced acute colitis. Taken together our results demonstrated that Arctigenin attenuates inflammation in DSS-induced acute colitis through suppression of NLRP3 inflammasome by SIRT1.
牛蒡子苷元（ARC-G）是从牛蒡子中提取的主要活性成分，具有广泛的药理作用。此外，已有研究表明ARC-G对炎症性疾病具有优异的疗效。本研究旨在明确牛蒡子苷元在葡聚糖硫酸钠（DSS）诱导的急性结肠炎中减轻炎症的功能，并确定其可能的机制。通过在饮用水中给予2.0% DSS诱导小鼠发生急性结肠炎。将急性结肠炎小鼠每天腹腔注射20 mg/kg牛蒡子苷元，持续7天。使用MPO活性试剂盒测量MPO活性水平。采用蛋白质免疫印迹分析来确定蛋白质表达。牛蒡子苷元可预防结肠炎并减轻DSS诱导的急性结肠炎中的炎症。在DSS诱导的急性结肠炎中，牛蒡子苷元通过SIRT1抑制NLRP3炎性小体。在LPS模型的THP-1细胞中，牛蒡子苷元通过SIRT1抑制NLRP3、caspase-1和IL-1β蛋白表达。Si-NLRP3增强了牛蒡子苷元对LPS模型THP-1细胞炎症的影响。Si-SIRT1减弱了牛蒡子苷元对LPS模型THP-1细胞炎症的影响。NLRP3抑制剂INF39也增强了牛蒡子苷元对DSS诱导的急性结肠炎炎症的影响。SIRT1抑制剂也减弱了牛蒡子苷元对DSS诱导的急性结肠炎炎症的影响。综上所述，我们的结果表明，牛蒡子苷元通过SIRT1抑制NLRP3炎性小体减轻DSS诱导的急性结肠炎中的炎症。
