异常子宫出血大鼠模型的构建与评价
连辉1, 姜艳玲1, 刘佳1, 张玉立2, 谢伟2, 薛晓鸥2, 李健1()()
Construction and Evaluation of a Rat Model of Abnormal Uterine Bleeding
LIAN Hui1, JIANG Yanling1, LIU Jia1, ZHANG Yuli2, XIE Wei2, XUE Xiaoou2, LI Jian1()()

图 4. 异常子宫出血模型大鼠的血清性激素水平、子宫血管和间质的损伤修复情况和血管收缩功能的变化
注:A,ELISA检测正常对照大鼠和异常子宫出血模型大鼠孕激素撤退36 h血清中性激素包括FSH、E2、LH和PROG的水平(n=6);B,免疫组织化学染色检测两组大鼠子宫组织中血管内皮表达蛋白即血小板-内皮细胞黏附分子-1(CD31)、血管生成蛋白即血管内皮生长因子(VEGF)、间质损伤和修复蛋白即基质金属蛋白酶-9(MMP-9)的表达及其结果分析(n=3,照片图比例尺为100 μm),以及大鼠子宫内膜TUNEL染色结果及其阳性细胞占比统计[n=3,低倍镜图片(比例尺为100 μm)中星号(*)标记为高倍镜(比例尺为25 μm)观察处];C,蛋白质印迹法检测两组大鼠子宫组织中成纤维细胞生长因子2(FGF2)和内皮素-1(ET-1)的表达及其相对量分析(n=3,数据表示为平均值±标准误;与正常对照组比较,nsP>0.05,*P<0.05,**P<0.01)。

Figure 4. Changes in serum sex hormone levels, injury and repair of uterus blood vessels and stroma, and vascular contractile function of uterus in abnormal uterine bleeding model rats
Note: A, ELISA was used to measure serum levels of sex hormones, including FSH, E2, LH, and PROG, in normal control rats and the AUB model rats at 36 h after progesterone withdrawal (n=6). B, Immunohistochemistry was performed to assess the expression of vascular endothelial marker platelet endothelial cell adhesion molecule-1 (CD31), angiogenesis-related protein vascular endothelial growth factor (VEGF), and stromal injury/repair protein matrix metalloproteinase-9 (MMP-9) in uterine tissues of both groups,along with statistical analysis of the results (n=3; scale bars: 100 μm). Additionally, TUNEL staining of rat endometrium was conducted, and the percentage of positive cells was quantified [n=3; asterisks (*) in low-magnification images (scale bars: 100 μm) indicate regions selected for high-magnification observation (scale bars: 25 μm)]. C, Western blotting was employed to detect the expression of fibroblast growth factor 2 (FGF2) and endothelin-1 (ET-1) in uterine tissues of both groups, along with relative quantification (n=3; data presented as mean ± standard error (SE); Compared with normal control group, nsP>0.05, *P<0.05, **P<0.01).