ubiquinone and Urinary-Bladder--Overactive

Competent detrusor muscles with coordinated contraction and relaxation are crucial for normal urinary bladder storage and emptying functions. Hence, detrusor instability, and subsequently bladder overactivity, may lead to undesirable outcomes including incontinence. Multiple mechanisms may underlie the pathogenesis of detrusor overactivity including inflammation and oxidative stress. Herein, we tested the possibility that CoQ10 may have a potential therapeutic role in detrusor overactivity.. Forty adult male Wistar albino rats weighing 100-150 g were used in the present study. Rats were divided (10/group) into control (receiving vehicles), monosodium glutamate (MSG)-treated (receiving 5 mg/kg MSG daily for 15 consecutive days), MSG + OO-treated (receiving concomitantly 5 mg/kg MSG and olive oil for 15 consecutive days), MSG + CoQ10-treated (receiving concomitantly 5 mg/kg MSG and 100 mg/kg CoQ10 daily for 15 consecutive days) groups.. MSG resulted in significant increase in bladder weight and sensitised the bladder smooth muscles to acetylcholine. MSG has also resulted in significant increase in bladder TNF-α, IL-6, malondialdehyde, nerve growth factor and connexion 43, with significant decrease in the antioxidant enzymes superoxide dismutase and catalase. Olive oil had no effect on MSG induced alterations of different parameters. Treatment with CoQ10 has resulted in a significant restoration of all the altered parameters.. Taken together, our results suggest that CoQ10 antagonizes the deleterious effects of MSG on detrusor activity. We propose that CoQ10 could be a therapeutic strategy targeting urinary bladder dysfunction.

Topics: Animals; Gap Junctions; Inflammation; Male; Muscle, Smooth; Oxidative Stress; Rats; Rats, Wistar; Sodium Glutamate; Ubiquinone; Urinary Bladder; Urinary Bladder, Overactive

We investigated the protective effects of coenzyme Q10 on bladder dysfunction in a rat model of atherosclerosis induced chronic bladder ischemia.. A total of 24 male Sprague-Dawley® rats at age 16 weeks were divided into 4 groups of 6 each, including group 1--untreated, sham operated rats, group 2--coenzyme Q10 treated, sham operated rats, group 3--untreated rats with chronic bladder ischemia and group 4--coenzyme Q10 treated rats with chronic bladder ischemia. Groups 3 and 4 received an endothelial injury to the iliac arteries and were fed a 2% cholesterol diet for 8 weeks. Groups 2 and 4 were treated with coenzyme Q10 and the others were treated with vehicle for 4 weeks. Eight weeks postoperatively we performed continuous in vivo cystometry, an in vitro detrusor muscle strip study and a malondialdehyde assay. Histological examination of the bladder walls and iliac arteries was also done.. In vivo cystometry revealed that coenzyme Q10 administration after the induction of chronic bladder ischemia prolonged micturition frequency and the intercontraction interval, and increased bladder capacity compared to those in untreated rats with chronic bladder ischemia. In the detrusor muscle strip study coenzyme Q10 administration after the induction of chronic bladder ischemia increased contractile responses compared to those in untreated rats with chronic bladder ischemia. Rats with chronic bladder ischemia also showed higher malondialdehyde in bladder tissue and serum than the other groups. Chronic bladder ischemia induced submucosal fibrosis of the bladder walls and a degenerative change in the blood vessel tunical media, as shown on histological examination.. Our study suggests that coenzyme Q10 acts as an antioxidant to protect bladder function in this chronic bladder ischemia model.

Topics: Animals; Biopsy, Needle; Chronic Disease; Disease Models, Animal; Immunohistochemistry; Ischemia; Male; Malondialdehyde; Muscle Contraction; Oxidative Stress; Protective Agents; Random Allocation; Rats; Rats, Sprague-Dawley; Reference Values; Sensitivity and Specificity; Ubiquinone; Urinary Bladder; Urinary Bladder, Overactive; Urodynamics