Epigallocatechin Gallate Attenuates Bladder Dysfunction via Suppression of Oxidative Stress in a Rat Model of Partial Bladder Outlet Obstruction

被引:20
作者
Gu, Meng [1 ]
Liu, Chong [1 ]
Wan, Xiang [1 ]
Yang, Tianye [2 ]
Chen, Yanbo [1 ]
Zhou, Juan [1 ]
Chen, Qi [1 ]
Wang, Zhong [1 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Med, Shanghai Peoples Hosp 9, Dept Urol, Shanghai 200011, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Shanghai Peoples Hosp 9, Dept Emergency, Shanghai 200011, Peoples R China
关键词
BENIGN PROSTATIC HYPERPLASIA; URINARY-TRACT SYMPTOMS; NATURAL-HISTORY; EGCG; ISCHEMIA; PATHWAY; NRF2; MEN;
D O I
10.1155/2018/1393641
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
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页数:10
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