Abstract
Postmenopausal women with ovary hormone deficiency (OHD) are subject to overactive bladder (OAB) symptoms. The present study attempted to elucidate whether low-intensity extracorporeal shock wave therapy (LiESWT) alters bladder angiogenesis, decreases inflammatory response, and ameliorates bladder hyperactivity to influence bladder function in OHD-induced OAB in human clinical trial and rat model. The ovariectomized (OVX) for 12 months Sprague–Dawley rat model mimicking the physiological condition of menopause was utilized to induce OAB and assess the potential therapeutic mechanism of LiESWT (0.12 mJ/mm2, 300 pulses, and 3 pulses/second). The randomized, single-blinded clinical trial was enrolled 58 participants to investigate the therapeutic efficacy of LiESWT (0.25 mJ/mm2, 3000 pulses, 3 pulses/second) on postmenopausal women with OAB. The results revealed that 8 weeks’ LiESWT inhibited interstitial fibrosis, promoted cell proliferation, enhanced angiogenesis protein expression, and elevated the protein phosphorylation of ErK1/2, P38, and Akt, leading to decreased urinary frequency, nocturia, urgency, urgency incontinence, and post-voided residual urine volume, but increased voided urine volume and the maximal flow rate of postmenopausal participants. In conclusion, LiESWT attenuated inflammatory responses, increased angiogenesis, and promoted proliferation and differentiation, thereby improved OAB symptoms, thereafter promoting social activity and the quality of life of postmenopausal participants.
Highlights
Postmenopausal women with ovary hormone deficiency (OHD) status could cause urological dysfunctions, including overactive bladder (OAB) symptoms, stress urinary incontinence (SUI), and recurrent urinary tract infection (UTI) [1]
Based on the above findings, we considered that low-intensity extracorporeal shock wave therapy (LiESWT) promoted bladder angiogenesis by increasing capillary density to improve OHD-induced pathological alteration, while this angiogenic enhancement was through VEGF/VEGF-R/MAPK (P38 and Erk1/2) pathways and Laminin/Integrin-α6/Akt pathways
3000 pulses, 3 Hz, and once/week) on OAB was analyzed by 3-day urinary diary,For uroflowmetry, postvoid residual urinary volume (PVR), and LiESWT
Summary
Postmenopausal women with ovary hormone deficiency (OHD) status could cause urological dysfunctions, including overactive bladder (OAB) symptoms, stress urinary incontinence (SUI), and recurrent urinary tract infection (UTI) [1]. Up to 45% of postmenopausal women with vaginal atrophy are associated with urogenital atrophy and urinary symptoms, including increased urinary frequency, nocturia, urgency, urgency incontinence, and recurrent UTI [2,3,4]. Epidemiological studies have shown that estrogen deficiency is associated with an increased risk of lower urinary tract symptoms (LUTSs) in ageing women [5]. Postmenopausal women with estrogen deficiency are usually reluctant to estrogen therapy due to fear of hormone related cancer: such as endometrial or breast malignancy [7].
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