Abstract
Metabolic syndrome (MetS) and ovarian hormone deficiency could affect bladder storage dysfunction. Epigallocatechin-3-gallate (EGCG), a polyphenolic compound in green tea, has been shown to protect against ovarian hormone deficiency induced overactive bladder (OAB). The present study investigated oxidative stress induced by MetS and bilateral ovariectomy (OVX), and elucidated the mechanism underlying the protective effect of EGCG (10 umol/kg/day) on bladder overactivity. Rats were fed with high fat high sugar (HFHS) diet to induce MetS and received ovariectomy surgery to deprive ovarian hormone. By dieting with HFHS for 6 months, rats developed MetS and OAB. MetS + OVX deteriorated bladder storage dysfunction more profound than MetS alone. MetS and MetS + OVX rats showed over-expression of inflammatory and fibrosis markers (1.7~3.8-fold of control). EGCG pretreatment alleviated storage dysfunction, and protected the bladders from MetS and OVX - induced interstitial fibrosis changes. Moreover, OVX exacerbated MetS related bladder apoptosis (2.3~4.5-fold of control; 1.8~2.6-fold of Mets group), enhances oxidative stress markers (3.6~4.3-fold of control; 1.8~2.2-fold of Mets group) and mitochondrial enzyme complexes subunits (1.8~3.7-fold of control; 1.5~3.4-fold of Mets group). EGCG pretreatment alleviated bladder apoptosis, attenuated oxidative stress, and reduced the mitochondrial and endoplasmic reticulum apoptotic signals. In conclusions, HFHS feeding and ovarian hormone deficiency enhances the generation of oxidative stress mediated through mitochondrial pathway. EGCG reduced the generation of oxidative stress and lessened bladder overactivity.
Highlights
Estrogen is a unique hormone that modulates various physiological conditions in females including voiding function[1]
Total 52 female Sprague-Dawley rats purchased from Animal Center of BioLASCO (Taipei, Taiwan) initially weighing 200–250 g were divided into five different groups: (a) normal rat chow diet group, (b) Metabolic syndrome (MetS) induced with the high fat and high sugar (HFHS) dieting group, (c) MetS induced with the high fat high sugar (HFHS) dieting plus bilateral OVX group, (d) MetS induced with the HFHS dieting plus bilateral OVX combined with EGCG (10 umol/kg/day) intraperitoneal (IP) injection group, and (e) MetS induced with the HFHS dieting combined with EGCG (10 umol/kg/day) IP injection group
The present study showed that both MetS and ovarian hormone deficiency affected bladder voiding dysfunction, including increasing micturition frequency and peak micturition pressure, diminishing bladder voided volume, and raising oxidative stress, which resulted in bladder damage and interstitial fibrosis
Summary
Estrogen is a unique hormone that modulates various physiological conditions in females including voiding function[1]. OVX was applied to mimic the physiological conditions of ovarian hormone deficiency and to induce bladder overactivity in a rat model. Our previous investigation demonstrated that ovarian hormone deficiency in the OVX rats resulted in diminishing bladder compliance, increasing oxidative damage and interstitial fibrosis, and enhancing bladder mucosa apotosis[6]. Both ovarian hormone deficiency and MetS have been associated with the bladder overactivity and lower urinary tract symptoms (LUTS)[7]. Mitochondrial function is considered relating to MetS associated oxidative stress[8], but the mechanisms of MetS and ovarian hormone deficiency in relation to bladder dysfunction are still not clearly elucidated. Decreasing oxidative stress as well as enhancing mitochondrial function might be important therapeutic strategies for MetS8
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