![]() Therefore, increased apoptosis may cause ECM remodeling and eventually result in the weakening of pelvic structures after various types of pelvic trauma, including pregnancy and vaginal delivery, pelvic surgery, or chronic abdominal pressure induced by chronic constipation. Apoptosis is involved in the pathogenesis and pathological process of many types of diseases, including extracellular matrix (ECM) remodeling after tissue injury. The nuclear translocation of Nrf2 can activate a series of antioxidant genes, such as glutathione peroxidase ( GPX), superoxide dismutase ( SOD), catalase ( CAT), and heme oxygenase-1 ( HO-1). Nuclear factor erythroid-2-related factor 2 (Nrf2) is a well-characterized global antioxidant gene inducer. Oxidative damage has been reported to be involved in mechanical trauma-induced PFD. Normal mechanical strain induces a physiological rise of ROS levels, while the excessive mechanical stress causes excessive ROS accumulation, eventually resulting in oxidative damage. Mechanical stress can induce the accumulation of reactive oxygen species (ROS). These data suggest that oxidative damage and apoptosis may contribute to PFD. Increased oxidative damage and apoptotic index have been reported in vaginal walls and pelvic connective tissues of PFD patients, especially in POP patients and patients with SUI induced by vaginal birth trauma or chronic abdominal pressure. This can cause traumatic slackness and alterations of the normal anatomical position and function of pelvic organs, resulting in SUI and/or POP. Vaginal delivery and chronic constipation or other causes of abdominal pressure increase the mechanical injury of pelvic connective tissues and muscular tissues. ![]() The vaginal wall plays an important role in maintaining the normal position and function of the vesical neck and urethra, which are attached to the anterior vaginal wall. The mechanical strength and toughness of the pelvic tissues are essential for maintaining the normal anatomical position and function of pelvic organs. The normal function of the female pelvic floor requires an intact anatomical structure, consisting of pelvic muscles, nerves, and connective tissues. Aging and vaginal delivery-induced pelvic injury are two of the most important risk factors of these disorders. Epidemiological studies indicate that SUI has significant adverse effects on women's everyday life and causes great economic burden. Stress urinary incontinence (SUI) is one of the most common types of PFD in women. Antioxidative therapy may be a promising treatment for mechanical trauma-related SUI.įemale pelvic floor dysfunction (PFD) is one of the most common benign gynecological diseases, which also include urinary incontinence (UI), pelvic organ prolapses (POP), and sexual dysfunction. Taken together, our data suggested that Nrf2 is a potential protective factor in mechanical trauma-induced apoptosis in a mouse model of SUI. The results showed that Nrf2 overexpression significantly alleviated VD-induced abnormalities in the anterior vaginal wall. To further confirm the role of Nrf2 in mechanical trauma-induced apoptosis and SUI, VD was performed on mice overexpressing Nrf2 via in vivo transfection of LV-Nfe2l2. The results showed that Nrf2 knockout aggravated VD-induced reduction in LPP, increase in cell apoptosis and peroxidation product levels, decrease in antioxidative protein activities, and alterations in apoptosis-related protein levels in the vaginal walls of mice. Leak point pressure (LPP) levels of apoptosis, apoptosis-related proteins, and peroxidation products and the activities of antioxidative proteins in the anterior vaginal wall were measured in wild-type (Nfe2l2 +/+) C57BL/6 mice and Nrf2-knockout mice (Nfe2l2 −/−). To test this hypothesis, a mouse model of vaginal distension- (VD-) induced SUI was established. Therefore, we predicted that Nrf2 may have a protective role in mechanical trauma-induced SUI. Nuclear factor erythroid-2-related factor 2 (Nrf2) is a well-characterized global antioxidant gene inducer that can reduce oxidative damage and apoptosis. Our previous results indicate that cell apoptosis and oxidative damage increase in a mouse model of mechanical injury-induced SUI and in fibroblasts treated with excessive mechanical strain. Apoptosis and oxidative damage are involved in the pathogenesis and progression of stress urinary incontinence (SUI).
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