Wang Qing, Wu Xiaotong, Wang Shiyan, Xie Bing, Sun Xiuli, Wang Jianliu
Department of Obstetrics and Gynecology, Peking University People's Hospital, No.11, Xi-Zhi-Men South Street, Xi Cheng District, Beijing, 100044, China.
The Key Laboratory of Female Pelvic Floor Disorders, Beijing, China.
Int Urogynecol J. 2024 Nov;35(11):2141-2152. doi: 10.1007/s00192-024-05943-9. Epub 2024 Oct 7.
Vaginal delivery and resulting pelvic floor muscle (PFM) dysfunction are significant risk factors for pelvic floor dysfunction (PFD). Despite this, the biological basis underlying PFD after childbirth remain unclear. This study was aimed at assessing the early response of the vaginal wall and PFM to simulated birth injury (SBI) in rats.
Forty female Sprague-Dawley rats were divided into four groups: control (sham operation), and 1, 4, and 14 days post-injury. In the SBI groups, a catheter was inserted into the vagina with 130 g of weight attached to the end, and the balloon was inflated to 5 ml for 2 h. Evaluation of vaginal tissues and PFMs included histological, immunohistochemical, Western blot, and uniaxial biomechanical testing.
In the vaginal wall, the SBI group showed significantly lower COL1A1 expression and higher MMP-2 and MMP-9 expression. At 4 and 14 days post-injury, there was a significant decrease in PFM fiber area and increased collagen content. The SBI group also exhibited significant increases in the expression of Nrf2, NQO1, HO-1, and SOD-2, indicating involvement of oxidative stress in both the vaginal wall and PFMs. Protein expression of Pax7 and MyoG, as well as the number of fibers with centralized nuclei, continued to increase significantly after SBI. Additionally, the vaginal wall of the SBI group showed a decreasing trend in tensile strength and elastic modulus, with a greater ultimate strain.
Extracellular matrix remodeling, oxidative stress, decreased biomechanical properties, and muscle dysmyogenesis may collectively contribute to increased susceptibility to PFD development.
阴道分娩及由此导致的盆底肌肉(PFM)功能障碍是盆底功能障碍(PFD)的重要危险因素。尽管如此,产后PFD的生物学基础仍不清楚。本研究旨在评估大鼠阴道壁和PFM对模拟分娩损伤(SBI)的早期反应。
40只雌性Sprague-Dawley大鼠分为四组:对照组(假手术),以及损伤后1天、4天和14天组。在SBI组中,将一根导管插入阴道,末端连接130克重物,将球囊充气至5毫升并保持2小时。对阴道组织和PFM的评估包括组织学、免疫组织化学、蛋白质免疫印迹和单轴生物力学测试。
在阴道壁中,SBI组COL1A1表达显著降低,MMP-2和MMP-9表达升高。在损伤后4天和14天,PFM纤维面积显著减小,胶原蛋白含量增加。SBI组Nrf2、NQO1、HO-1和SOD-2的表达也显著增加,表明氧化应激参与了阴道壁和PFM的变化。SBI后,Pax7和MyoG的蛋白表达以及具有中央核的纤维数量持续显著增加。此外,SBI组阴道壁的抗张强度和弹性模量呈下降趋势,极限应变更大。
细胞外基质重塑、氧化应激、生物力学性能下降和肌肉发育异常可能共同导致PFD发生易感性增加。