血小板应答蛋白1在双侧卵巢切除大鼠阴道壁中的表达

目的 通过检测大鼠雌激素缺乏模型中阴道壁胶原纤维的形态结构及血小板应答蛋白1（thrombospondin-1,THBS1）的表达,探讨THBS1在雌激素缺乏诱导的大鼠阴道壁过度纤维化中的作用。方法 3月龄未生产过的SD大鼠24只,随机分为假手术组和实验组,每组各12只。造模12周后处死大鼠,取阴道壁进行分析。Masson染色观察大鼠阴道壁胶原纤维的形态结构变化,免疫组织化学染色法和蛋白质印迹法检测THBS1蛋白的表达水平。结果 造模12周后,实验组大鼠子宫萎缩明显,体质量增加显著高于假手术组,雌二醇水平显著低于假手术组（P<0.01）。与假手术组比较,实验组大鼠的阴道壁上皮层明显萎缩,平滑肌束变薄,肌束间隙变宽,固有层和肌层中胶原纤维沉积增加,且排列分布紊乱碎片化。实验组大鼠阴道壁中THBS1表达显著高于假手术组（P<0.05）。结论 雌激素缺乏可通过上调THBS1表达介导阴道壁过度纤维化,进而损害阴道壁的生物力学性质,导致其对盆腔脏器脱垂的易感性增加。

Expression of thrombospondin-1 in vaginal wall of bilateral ovariectomy rats

Objective To explore the possible role of thrombospondin-1 (THBS1) in the excessive fibrosis of vaginal wall induced by estrogen deficiency in rats, the morphological structure of collagen fibers and the expression of THBS1 in the vaginal wall were detected in the estrogen deficiency model of rats. Methods Twenty-four SD rats aged 3 months without delivery were randomly divided into sham operation group and experimental group, with 12 rats in each group. After 12 weeks of modeling, the rats were killed and the vaginal walls were taken for analysis. Masson staining was used to observe the morphological and structural changes of collagen fibers in vaginal wall of rats. Immunohistochemical staining and Western blotting were used to detect the expression level of THBS1 protein. Results After 12 weeks of modeling, the uterine atrophy of experimental group was obvious, the increase of body mass was significantly higher than that of sham operation group, and the level of estradiol was significantly lower than that of sham operation group (P<0.01). Compared with the sham operation group, the upper cortex of vaginal wall of experimental group was significantly atrophy, the smooth muscle bundles were thinner, the muscle gap was wider, the collagen fiber deposition in lamina propria and muscle layer was increased, and the arrangement and distribution were disordered and fragmented. THBS1 expression in vaginal wall of experimental group was significantly higher than that of sham operation group (P<0.05). Conclusion Estrogen deficiency may mediate excessive fibrosis of vaginal wall by upregulating THBS1 expression, thereby damaging the biomechanical properties of vaginal wall and leading to an increased susceptibility to pelvic organ prolapse development.