Abstract
Purpose To investigate the protective effect of epigallocatechin gallate (EGCG), a green tea extract, and its underlying mechanism on bladder dysfunction in a rat model of bladder outlet obstruction (BOO). Materials and Methods Sprague-Dawley rats of BOO were surgically induced and followed by treatment with EGCG (5 mg/kg/day) or saline (control) via intraperitoneal injection. Cystometry was performed on four weeks postoperatively in conscious rats. H&E, Masson trichrome, and TUNEL staining were performed to observe tissue alterations. Oxidative stress markers were measured, and protein expression of Nrf2-ARE pathway was examined by immunohistochemistry and Western blotting. Results Our data showed that EGCG could increase the peak voiding pressure and bladder compliance and prolong micturition interval of BOO rats compared with control and finally reduce the frequency of urinary. EGCG could ameliorate the increase of collagen fibers and ROS induced by obstruction and increase the activity of SOD, GSH-Px, and CAT. The level of cell apoptosis was decreased in BOO rats treated with EGCG compared with control, and caspase-3 expression was reduced as well. Moreover, EGCG could activate the Nrf2 expression with elevation of its target antioxidant proteins. Conclusions EGCG alleviates BOO-induced bladder dysfunction via suppression of oxidative stress and activation of the protein expression of Nrf2-ARE pathway.
Highlights
Benign prostatic hyperplasia (BPH) characterized by gradually nonmalignant enlargement of prostate gland [1, 2] is a very common chronic disease in elderly men
Based on our previous study [10] that demonstrated the decrease of oxidative stress and activation of the Nrf2ARE pathway may ameliorate bladder dysfunction induced by bladder outlet obstruction (BOO), we explored the ability of epigallocatechin gallate (EGCG) to ameliorate bladder dysfunction by inhibiting oxidative stress via the regulation of the nuclear erythroid-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway in a rat model of BOO in the present study
As investigated in animal models, chronic bladder ischemia might produce oxidative leading to denervation of the bladder and the expression of tissue-damaging molecules in the bladder wall, which could be responsible for the development of bladder hyperactivity progressing to bladder underactivity
Summary
Benign prostatic hyperplasia (BPH) characterized by gradually nonmalignant enlargement of prostate gland [1, 2] is a very common chronic disease in elderly men. Production of high levels of ROS causes a significant decrease in antioxidant defense mechanisms leading to protein, lipid, and DNA damage and subsequent disruption of cellular functions and Oxidative Medicine and Cellular Longevity cell death but at lower levels induce subtle changes in intracellular signaling pathways. Nuclear erythroid-related factor 2 (Nrf2) could promote expression of antioxidative genes through the antioxidant response element (ARE) to regulate cellular antioxidative responses and redox status [9]. It has been established in the literature that activation of the Nrf2-ARE pathway may ameliorate bladder dysfunction caused by bladder outlet obstruction [10]
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