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Updated: Jun 11, 2025
Biaxial Basal Tone and Passive Testing of the Murine Reproductive System Using a Pressure Myograph
Published on: August 13, 2019
Mechanical Stress-Oxidative Stress Axis: Biological Basis in the Vaginal Wall and Pelvic Floor Muscles of Rats with
Qing Wang1,2,3, Xiaotong Wu1,2,3, Shiyan Wang1,2,3
1Department of Obstetrics and Gynecology, Peking University People's Hospital, No.11, Xi-Zhi-Men South Street, Xi Cheng District, Beijing, 100044, China.
Introduction And Hypothesis:
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.
Methods:
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.
Results:
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.
Conclusion:
Extracellular matrix remodeling, oxidative stress, decreased biomechanical properties, and muscle dysmyogenesis may collectively contribute to increased susceptibility to PFD development.
