Department of Anorectal, Yangzhou Traditional Chinese Medicine Hospital Affiliated to Nanjing University of Chinese Medicine, Yangzhou, China.
The Third Clinical Medicine College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China.
Hum Exp Toxicol. 2022 Jan-Dec;41:9603271221078866. doi: 10.1177/09603271221078866.
Due to its well-known anti-inflammatory property, oxymatrine (OMT) has received more attention on the aspect of treating ulcerative colitis. Although efforts have been undertaken to understand the therapeutic mechanism of OMT on ulcerative colitis (UC), the remedial principle is still ambiguous. Numerous studies have shown that TLR9/Myd88/NF-κB signal pathway played a key role in the pathogenesis of UC. Moreover, TLR9/Myd88/NF-κB signal pathway is a part of the most important pathways for regulating the immune response. We explored the influence of OMT with different dosages on UC by establishing a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Moreover, the participation of TLR9/Myd88/NF-κB signal pathway and whether OMT protects against UC though targeting this pathway are further studied. Our data revealed that OMT could significantly relieve the symptom of TNBS-induced colitis in rats by reactivating the tight junction protein and, more important, by inhibiting the activation of TLR9/Myd88/NF-κB pathway and protein expression levels of its downstream inflammatory factors. OMT could relieve colitis in rat models by impacting tight junction proteins' TLR9/Myd88/NF-κB signal pathways and activity.
由于其众所周知的抗炎特性，氧化苦参碱（OMT）在治疗溃疡性结肠炎方面受到了更多关注。尽管已经努力了解 OMT 治疗溃疡性结肠炎（UC）的治疗机制，但治疗原理仍不清楚。许多研究表明，TLR9/Myd88/NF-κB 信号通路在 UC 的发病机制中起关键作用。此外，TLR9/Myd88/NF-κB 信号通路是调节免疫反应的最重要途径之一。我们通过建立 2,4,6-三硝基苯磺酸（TNBS）诱导的结肠炎模型，探讨了不同剂量的 OMT 对 UC 的影响。此外，进一步研究了 TLR9/Myd88/NF-κB 信号通路的参与情况，以及 OMT 是否通过靶向该通路来保护 UC。我们的数据表明，OMT 通过重新激活紧密连接蛋白，更重要的是通过抑制 TLR9/Myd88/NF-κB 通路的激活及其下游炎症因子的蛋白表达水平，可显著缓解 TNBS 诱导的结肠炎大鼠的症状。OMT 可通过影响紧密连接蛋白的 TLR9/Myd88/NF-κB 信号通路和活性来缓解大鼠结肠炎。
