In this study, we aimed to explore the effect of TrkB-PLC/IP3 pathway on intestinal inflammatory factors and enterocyte apoptosis in mice with colitis. The mouse model of ulcerative colitis was established by medication, and 40 SPF C57BL/6J mice (8 weeks old) were randomly divided into normal group (healthy mice, n = 10), control group (sham-operated mice, n = 10), model group (model mice without any treatment, n = 10), and K252a group (model mice treated with 100 μmol/kg TrkB-PLC/IP3 pathway inhibitor for 5 days before clysis, n = 10). The results showed that mice in the model and K252a groups, as compared with normal and control groups, had no significant changes in the levels and protein expressions of serum tumor necrosis factor-α (TNF-α) and TNF-γ in the colon tissues (P>0.05), and had a significant increase in disease activity index, colon mucosa damage index, tissue damage index scores, and levels and protein expressions of serum interleukin-4 (IL-4) and IL-8, but had a significant decrease in the level and protein expression of serum IL-10 (P<0.05). Mice in the model and K252a groups showed blocked enterocyte cycle progression, elevated apoptosis ratio, and significantly increased mRNA and protein expressions of Caspase3, Bax, FasL, and Fas, but significantly reduced mRNA and protein expressions of p-TrkB, PLC-γ1, IP3, and Bcl-2 (P<0.05). Moreover, intestinal inflammation and apoptosis induced by colitis in the K252a group became more aggravated by inhibiting the activity of TrkB-PLC/IP3 pathway. In conclusion, inhibition of TrkB-PLC/IP3 pathway can increase the expression of intestinal inflammatory factors and promote enterocyte apoptosis in mice with colitis.

中文翻译：

---

TrkB-PLC / IP3通路对结肠炎小鼠肠道炎症因子和肠细胞凋亡的影响。

在这项研究中，我们旨在探讨TrkB-PLC / IP3途径对结肠炎小鼠肠道炎症因子和肠细胞凋亡的影响。通过药物治疗建立溃疡性结肠炎的小鼠模型，将40只SPF C57BL / 6J小鼠（8周龄）随机分为正常组（健康小鼠，n  = 10），对照组（假手术小鼠，n  = 10）。 ，模型组（未经任何处理的模型小鼠，n  = 10）和K252a组（在裂解前用100μmol/ kg TrkB-PLC / IP3途径抑制剂治疗5天的模型小鼠，n = 10）。结果表明，模型组和K252a组的小鼠与正常组和对照组相比，结肠组织中血清肿瘤坏死因子-α（TNF-α）和TNF-γ的水平和蛋白表达无明显变化（P > 0.05），且疾病活动指数，结肠粘膜损伤指数，组织损伤指数得分以及血清白介素-4（IL-4）和IL-8的水平和蛋白质表达均显着增加，但具有显着性降低血清IL-10（P<0.05）。模型和K252a组的小鼠显示出肠细胞周期进程受阻，凋亡率升高，Caspase3，Bax，FasL和Fas的mRNA和蛋白表达显着增加，但p-TrkB，PLC-γ1的mRNA和蛋白表达显着降低， IP3和Bcl-2（P <0.05）。而且，通过抑制TrkB-PLC / IP3途径的活性，K252a组中由结肠炎引起的肠炎症和细胞凋亡变得更加严重。总之，抑制TrkB-PLC / IP3通路可以增加结肠炎小鼠肠道炎症因子的表达并促进肠细胞的凋亡。