Liang Meng-di, Liang Yue-Run, Cheng Jin, Yang Ya-Ping, Xia Xuan, Yang Wen-Zhe, Hao Jie-Jie
Ministry of Education Key Laboratory of Marine Drugs,School of Medicine and Pharmacy, Ocean University of China Qingdao 266005,China.
Marine Biomedical Research Institute of Qingdao Qingdao 266100, China.
Zhongguo Zhong Yao Za Zhi. 2025 May;50(10):2778-2786. doi: 10.19540/j.cnki.cjcmm.20250103.705.
To study the therapeutic effect and mechanisms of ethyl syringate(MD) on ulcerative colitis(UC), the MTT assay was used to detect the proliferation inhibition of RAW264.7 cells and HT-29 cells by different concentrations of MD(50, 100, 200, 400 μmol·L(-1)). UC cell models were constructed by inducing RAW264.7 cells and HT-29 cells with lipopolysaccharide(LPS) and tumor necrosis factor-α(TNF-α). An animal model was established by inducing mice with 2.5% dextran sulfate sodium(DSS) to verify the therapeutic effect of MD on UC. A control group, a model group(LPS or TNF-α), and groups treated with different concentrations of MD(50, 100, 200, 400 μmol·L(-1)) were set up in this study. Nitric oxide(NO) levels were measured using a NO detection kit. Intracellular reactive oxygen species(ROS) levels were assessed using a laser confocal microscope and ROS kit. Enzyme-linked immunosorbent assay(ELISA) was used to detect changes in the levels of interleukin-6(IL-6), TNF-α, interferon-γ(INF-γ), interleukin-10(IL-10), and myeloperoxidase(MPO) in cells and animal tissues. Western blot was used to detect the expression levels of phosphorylated Janus kinase 2(p-JAK2), Janus kinase 2(JAK2), phosphorylated signal transducer and activator of transcription 3(p-STAT3), signal transducer and activator of transcription 3(STAT3), zonula occludens-1(ZO-1), occludin, and claudin-1 in cells and animal tissues. The results showed that MD can improve the inflammatory response by inhibiting the production of NO and ROS and regulating the expression of inflammatory factors. It significantly reduced the disease activity index(DAI) in mice, improved the shortening of the colon, and repaired intestinal epithelial damage by inhibiting the activation of the JAK2/STAT3 pathway, thereby exerting anti-UC activity.
为研究丁香酸乙酯（MD）对溃疡性结肠炎（UC）的治疗作用及机制，采用MTT法检测不同浓度MD（50、100、200、400 μmol·L⁻¹）对RAW264.7细胞和HT - 29细胞增殖的抑制作用。通过用脂多糖（LPS）和肿瘤坏死因子-α（TNF-α）诱导RAW264.7细胞和HT - 29细胞构建UC细胞模型。通过用2.5%葡聚糖硫酸钠（DSS）诱导小鼠建立动物模型，以验证MD对UC的治疗效果。本研究设立了对照组、模型组（LPS或TNF-α）以及用不同浓度MD（50、100、200、400 μmol·L⁻¹）处理的组。使用NO检测试剂盒测量一氧化氮（NO）水平。使用激光共聚焦显微镜和ROS试剂盒评估细胞内活性氧（ROS）水平。采用酶联免疫吸附测定（ELISA）检测细胞和动物组织中白细胞介素-6（IL - 6）、TNF-α、干扰素-γ（INF - γ）、白细胞介素-10（IL - 10）和髓过氧化物酶（MPO）水平的变化。采用蛋白质免疫印迹法检测细胞和动物组织中磷酸化的Janus激酶2（p - JAK2）、Janus激酶2（JAK2）、磷酸化信号转导子和转录激活子3（p - STAT3）、信号转导子和转录激活子3（STAT3）、紧密连接蛋白-1（ZO - 1）、闭合蛋白和Claudin - 1的表达水平。结果表明，MD可通过抑制NO和ROS的产生以及调节炎症因子的表达来改善炎症反应。它显著降低了小鼠的疾病活动指数（DAI），改善了结肠缩短情况，并通过抑制JAK2/STAT3通路的激活修复肠道上皮损伤，从而发挥抗UC活性。
