肝螺杆菌感染引起VDR-/-小鼠炎性肠病相关肠纤维化模型的建立及机制探讨
吴志浩1(), 曹舒扬2, 周正宇1()()
Establishment of an Intestinal Fibrosis Model Associated with Inflammatory Bowel Disease in VDR-/- Mice Induced by Helicobacter hepaticus Infection and Mechanism Exploration
WU Zhihao1(), CAO Shuyang2, ZHOU Zhengyu1()()

图5. H.hepaticus感染小鼠16周后结肠组织mRNA表达水平检测（A）、IL-33免疫组织化学染色（B）和蛋白质印迹（C）
注：RT-PCR检测显示，与WT小鼠感染组相比，VDR-/-小鼠感染组促炎因子和促纤维化因子转录水平显著升高（****P＜0.000 1，n=5）；免疫组织化学和蛋白质印迹也发现纤维化相关蛋白如IL-33和α-SMA表达的上调（**P<0.01，***P<0.001）。图B中放大倍数为200，比例尺为100 μm。

Figure 5. Detection of mRNA expression levels in colon tissue of mice infected with H. hepaticus after 16 weeks （A）， IL-33 immunohistochemical staining （B）， and Western blotting （C）
Note： RT-PCR showed that， compared to the WT+H.h group， the transcription levels of pro-inflammatory and pro-fibrotic factors were significantly elevated in the VDR-/-+H.h group （****P＜0.000 1，n=5）. Immunohistochemistry and Western blotting also revealed an upregulation of fibrosis-related proteins such as IL-33 and α-SMA （**P<0.01， ***P<0.001）. In Figure B， the magnification is ×200， and the scale bar is 100 μm.