Xu Linxia, Liu Wei, Huang Xixiang, Sun Tong, Mei Letian, Liu Man, Ren Zhi, Wang Meng, Zheng Hailun, Wang Qiangwu, Li Dapeng, Wang Qizhi, Ke Xiquan
Department of Gastroenterology, the First Affiliated Hospital of Bengbu Medical University, No. 287, Changhuai Road, Bengbu, Anhui, 233000, China.
BMC Gastroenterol. 2024 Dec 18;24(1):451. doi: 10.1186/s12876-024-03546-8.
To study the therapeutic effect of sinomenine hydrochloride (SH) on dextran sodium sulfate (DSS)-induced colitis in mice as an animal model and the changes of Notch signaling pathway in colon tissue of mice after treatment.
Twenty-four mice were randomly divided into control group, model group, SH low-dose group (20 mg/kg) and SH high-dose group (60 mg/kg), with 6 mice in each group. Disease activity index (DAI), colonic mucosal injury index and colonic histopathological score were calculated. The expression levels of related genes, proteins in Notch signaling pathway and inflammatory factors were quantified.
SH can significantly reduce the symptoms of colitis mice, and can significantly reduce the DAI score (Model: 3.44 ± 0.27; SH-20: 2.50 ± 0.18; SH-60: 1.89 ± 0.17; P < 0.001) and histopathological injury degree (Model: 7.67 ± 0.52; SH-20: 5.17 ± 0.75, P < 0.01; SH-60: 3.33 ± 0.52, P < 0.001). SH can down-regulate the expression levels of Notch1, NICD1, Jagged1 and Hes1 proteins in colon tissue of colitis mice (Model: 1.92 ± 0.16, 1.83 ± 0.21, 2.23 ± 0.22, 1.91 ± 0.17; SH-20: 1.56 ± 0.12, 1.39 ± 0.13, 1.58 ± 0.12, 1.38 ± 0.11; SH-60: 1.24 ± 0.09, 1.23 ± 0.10, 1.23 ± 0.11, 1.22 ± 0.09; P < 0.01), and reduce the contents of serum pro-inflammatory cytokines TNF-α, IL-1β and IL-6 (Model: 718.53 ± 81.81, 51.62 ± 2.80, 444.07 ± 67.77; SH-20: 544.72 ± 90.03, 34.10 ± 2.90, 345.43 ± 43.40; SH-60: 434.11 ± 71.75, 29.44 ± 3.70, 236.11 ± 29.35; P < 0.001).
The therapeutic effect of SH on DSS-induced colitis in mice may be related to inhibiting the overactivation of Notch signaling pathway.
以小鼠为动物模型，研究盐酸青藤碱（SH）对葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎的治疗作用及治疗后小鼠结肠组织中Notch信号通路的变化。
将24只小鼠随机分为对照组、模型组、SH低剂量组（20mg/kg）和SH高剂量组（60mg/kg），每组6只。计算疾病活动指数（DAI）、结肠黏膜损伤指数和结肠组织病理学评分。定量Notch信号通路相关基因、蛋白及炎症因子的表达水平。
SH可显著减轻结肠炎小鼠的症状，并能显著降低DAI评分（模型组：3.44±0.27；SH-20组：2.50±0.18；SH-60组：1.89±0.17；P<0.001）和组织病理学损伤程度（模型组：7.67±0.52；SH-20组：5.17±0.75，P<0.01；SH-60组：3.33±0.52，P<0.001）。SH可下调结肠炎小鼠结肠组织中Notch1、NICD1、Jagged1和Hes1蛋白的表达水平（模型组：1.92±0.16、1.83±0.21、2.23±0.22、1.91±0.17；SH-20组：1.56±0.12、1.39±0.13、1.58±0.12、1.38±0.11；SH-60组：1.24±0.09、1.23±0.10、1.23±0.11、1.22±0.09；P<0.01），并降低血清促炎细胞因子TNF-α、IL-1β和IL-6的含量（模型组：718.53±81.81、51.62±2.80、444.07±67.77；SH-20组：544.72±90.03、34.10±2.90、345.43±43.40；SH-60组：434.11±71.75、29.44±3.70、236.11±29.35；P<0.001）。
SH对DSS诱导的小鼠结肠炎的治疗作用可能与抑制Notch信号通路的过度激活有关。
