Archives of gynecology and obstetrics · 2022
Application of estrogen for the treatment of stress urinary incontinence in mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Li Lu, Hong Shasha, Li Yang, Li Xiang, Yang Lian, Liu Jianfeng, Hong Li
Аннотация
BACKGROUND: Stress urinary incontinence (SUI) is a pervasive health tissue among women, which seriously affects the quality of life. The etiology of SUI is complex and diverse in women, with past studies having demonstrated that estrogen deficiency plays an important role in pelvic floor muscle atrophy and urethral degeneration. We comprehensively investigated the effects of estrogen in the treatment of SUI in female mice at cellular and animal levels.
METHODS: L929 fibroblasts mechanical injury model was established by four-point bending device, and SUI mouse model was established by vaginal dilation method commonly used to simulate labor injury. After estrogen treatment, the expressions of Collagen I, Collagen III, Elastin, TIMP-1, TIMP-2, MMP-2, and MMP-9 were detected, the leak point pressure (LPP) and abdominal leak point pressure (ALPP) of mice in each group were detected, and both the effect of estrogen on extracellular matrix remodeling of mouse urethra and anterior vaginal wall was observed from the histological level.
RESULTS: The results revealed that an appropriate amount of estrogen can promote the expression of Collagen I, Collagen III, Elastin, TIMP-1, and TIMP-2, decrease the expression of MMP-2 and MMP-9, and maintain the dynamic balance of MMPs/TIMPs at both cellular and animal levels. Meanwhile, we determined that estrogen can increase the LPP and ALPP values of SUI mice. The collagen fibers' content in the mice treated with estrogen was significantly greater than in the control group mice.
CONCLUSIONS: The estrogen may alleviate the symptoms of SUI by reconstituting ECM, thus laying a solid foundation for further exploration of estrogen therapy.
METHODS: L929 fibroblasts mechanical injury model was established by four-point bending device, and SUI mouse model was established by vaginal dilation method commonly used to simulate labor injury. After estrogen treatment, the expressions of Collagen I, Collagen III, Elastin, TIMP-1, TIMP-2, MMP-2, and MMP-9 were detected, the leak point pressure (LPP) and abdominal leak point pressure (ALPP) of mice in each group were detected, and both the effect of estrogen on extracellular matrix remodeling of mouse urethra and anterior vaginal wall was observed from the histological level.
RESULTS: The results revealed that an appropriate amount of estrogen can promote the expression of Collagen I, Collagen III, Elastin, TIMP-1, and TIMP-2, decrease the expression of MMP-2 and MMP-9, and maintain the dynamic balance of MMPs/TIMPs at both cellular and animal levels. Meanwhile, we determined that estrogen can increase the LPP and ALPP values of SUI mice. The collagen fibers' content in the mice treated with estrogen was significantly greater than in the control group mice.
CONCLUSIONS: The estrogen may alleviate the symptoms of SUI by reconstituting ECM, thus laying a solid foundation for further exploration of estrogen therapy.