Zhang Yongli, Liu Jiali, Zhang Dan, Qian Haihua
Department of Anorectal Surgery, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China.
Department of Anorectal Surgery, Xi'an Hospital of Traditional Chinese Medicine, Xi'an, Shaanxi, 710016, People's Republic of China.
Drug Des Devel Ther. 2025 Apr 26;19:3253-3268. doi: 10.2147/DDDT.S503483. eCollection 2025.
LianChuang ZhiXue Liquid (LCZXL) enema, one of the classic Chinese medicine prescriptions, in which herbal decoction enema acts directly on the intestines, is clinically effective in patients with ulcerative colitis (UC). However, its specific molecular mechanism has not been clarified to explore the underlying macular mechanism of LCZXL enema effect on UC, based on Jagged-1/Notch1 signaling pathway and the macrophage polarization.
After modeling of UC mice, the experiment was conducted in two parts: Experiment I: Control, Model, Mesalazine, Low dose of LCZXL (LCZXL-L), High dose of LCZXL (LCZXL-H); Weight and Disease Activity Index (DAI) scores were recorded on days 1, 3, 5, 7, 9, 11, and 13. On day 14, the colon was taken off. Then the colon length was measured and the damage index (CMDI) score of colon mucosal was evaluated. Zonula occludens-1 (Zo-1) Immunohistochemistry (IHC) and Hematoxylin-Eosin (HE) staining were performed to visualize the colon injury. ELISA was used to detect cytokines content in serum. The M1 and M2 markers and Jagged-1/Notch1 signaling pathway-related genes/proteins were quantified by IF double staining, PCR, WB, and flow cytometry. Experiment II: Control, Model, Recombinant mouse Jagged-1 protein/ Fc Chimera Active (Jagged-1/Fc), LCZXL, Jagged-1/Fc+LCZXL. The M1 and M2 markers and Jagged-1 proteins were quantified by WB, and flow cytometry.
Our results indicated that LCZXL could reduce the colon injury of UC mice effectively, which expressed DAI and CMDI score reduction, and inhibited colon structure damage. DSS induced a significant up-regulation of CD86, iNOS, TNF-α, IL-1β, and IL-6, and a down-regulation of Arg1, CD206, IL-4, IL-10 and increase of Jagged-1, Notch1, and Notch2. LCZXL enema treatment inhibiting the increase of UC modeling-induced CD86, TNF-α, IL-1β, and IL-6 and increased CD206, Arg1, IL-4, and IL-10 expression level. Notch signaling pathway activator Jagged-1/Fc aggravated M1 macrophage polarization and activated the Jagged-1/Notch1 signaling pathway. LCZXL treatment reversed this situation stop the activation of the Jagged-1/Notch1 signaling pathway.
Our study proved that LCZXL Enema could inhibit the M1 Macrophage Polarization and promote M2 macrophage polarization of ulcerative colitis via regulating the Jagged-1/Notch1 signaling pathway.
联创痔血合剂(LCZXL)灌肠剂是经典的中药方剂之一,其中中药汤剂灌肠直接作用于肠道,对溃疡性结肠炎(UC)患者临床疗效显著。然而,其具体分子机制尚未阐明。基于Jagged-1/Notch1信号通路和巨噬细胞极化,探讨LCZXL灌肠剂治疗UC的潜在机制。
建立UC小鼠模型后,实验分为两部分:实验一:对照组、模型组、美沙拉嗪组、低剂量LCZXL组(LCZXL-L)、高剂量LCZXL组(LCZXL-H);于第1、3、5、7、9、11和13天记录体重和疾病活动指数(DAI)评分。第14天,取出结肠,测量结肠长度并评估结肠黏膜损伤指数(CMDI)评分。进行紧密连接蛋白-1(Zo-1)免疫组织化学(IHC)和苏木精-伊红(HE)染色以观察结肠损伤情况。采用酶联免疫吸附测定(ELISA)检测血清中细胞因子含量。通过免疫荧光双染、聚合酶链反应(PCR)、蛋白质免疫印迹法(WB)和流式细胞术对M1和M2标志物以及Jagged-1/Notch1信号通路相关基因/蛋白进行定量分析。实验二:对照组、模型组、重组小鼠Jagged-1蛋白/Fc嵌合体活性片段(Jagged-1/Fc)、LCZXL组、Jagged-1/Fc+LCZXL组。通过WB和流式细胞术对M1和M2标志物以及Jagged-1蛋白进行定量分析。
结果表明,LCZXL可有效减轻UC小鼠的结肠损伤,表现为DAI和CMDI评分降低,抑制结肠结构损伤。葡聚糖硫酸钠(DSS)诱导CD86、诱导型一氧化氮合酶(iNOS)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)显著上调,精氨酸酶1(Arg1)、CD206、白细胞介素-4(IL-4)、白细胞介素-10(IL-10)下调,Jagged-1、Notch1和Notch2增加。LCZXL灌肠治疗抑制了UC建模诱导的CD86、TNF-α、IL-1β和IL-6增加,并提高了CD206、Arg1、IL-4和IL-10的表达水平。Notch信号通路激活剂Jagged-1/Fc加重M1巨噬细胞极化并激活Jagged-1/Notch1信号通路。LCZXL治疗逆转了这种情况,阻止了Jagged-1/Notch1信号通路的激活。
本研究证明,LCZXL灌肠剂可通过调节Jagged-1/Notch1信号通路抑制溃疡性结肠炎的M1巨噬细胞极化并促进M2巨噬细胞极化。