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3. 小鼠感染H.hepaticus后的肠道载菌量（A）和结肠组织HAI评分（B）
注：VDR-/-小鼠感染组的H. hepaticus肠道载菌量显著高于WT小鼠感染组（**P<0.01，n=5）。组织学活动指数评分显示，H.hepaticus感染引起结肠病变，并且VDR缺陷加重了结肠病变（*P<0.05，***P<0.001，****P<0.000 1，n=5）。

Figure 3. Colonic bacterial colonization （A） and HAI score of colon tissues （B） in mice infected with H.hepaticus
Note：The intestinal colonization of H.hepaticus was significantly higher in the VDR-/-+H.h group compared to the WT+H.h group（**P<0.01， n=5）. Histological activity index showed that the infection with H.hepaticus induced colonic pathology， while VDR deficiency exacerbated the pathological changes in the colon（*P<0.05， ***P<0.001， ****P<0.000 1， n=5）.