Epigallocatechin Gallate Attenuates Partial Bladder Outlet Obstruction-induced Bladder Injury via Suppression of Endoplasmic Reticulum Stress-related Apoptosis-In Vivo Study

被引:9
作者
Hsieh, Ju-Ton
Kuo, Kuan-Lin
Liu, Shing-Hwa
Shi, Chung-Sheng
Chang, Hong-Chiang
Lin, Wei-Chou
Chou, Chien-Tso
Hsu, Chen-Hsun
Liao, Shih-Ming
Wang, Zuo-He
Li, Chih-Chien
Huang, Kuo-How
机构
[1] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Dept Urol, Taipei 10764, Taiwan
[2] Natl Taiwan Univ, Coll Med, Taipei 10764, Taiwan
[3] Natl Taiwan Univ, Coll Med, Grad Inst Toxicol, Taipei 10764, Taiwan
[4] Chang Gung Univ, Coll Med, Grad Inst Clin Med Sci, Taoyuan, Taiwan
[5] Chang Gung Mem Hosp, Dept Med Res, Chiayi, Taiwan
[6] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Dept Pathol, Taipei 10764, Taiwan
关键词
RABBIT URINARY-BLADDER; GREEN TEA POLYPHENOLS; BLOOD-FLOW CHANGES; MICE; RAT; EXPRESSION; MORPHOLOGY; CATECHINS; HEART; MODEL;
D O I
10.1016/j.urology.2015.12.020
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVES To investigate the protective effect of epigallocatechin gallate (EGCG), a green tea extract, on partial bladder outlet obstruction (pBOO)-induced bladder injury in a rat model. METHODS The female Sprague-Dawley rats underwent sham or BOO procedures, and were divided into several groups (sham with saline injection, sham with EGCG treatment, BOO with saline injection, and BOO with EGCG treatment). The rats in each group were randomized into 2 groups (48 hours and 30 days after the BOO procedure) for when their bladders were harvested. EGCG (4.5 mg/kg/day) and saline were administered via intraperitoneal injection after the BOO procedure during the study period. Bladder tissue was examined for inflammation, endoplasmic reticulum (ER) stress-related apoptotic markers by Western blot, and histological staining. RESULTS BOO induced acute bladder injury (hemorrhage, edema, and neutrophil infiltration) after 48 hours. In addition, cystometry showed a decrease in micturition pressure and intercontractile interval. We also observed increased expressions of cyclooxygenase-2, poly(ADP-ribose) polymerase at 48 hours, as well as ER stress markers such as caspase-12 and CCAAT/-enhancer-binding protein homologous protein (CHOP). Treatment with EGCG significantly improved pBOO-induced histologic changes, bladder dysfunction, and the overexpression of cyclooxygenase-2, CHOP, and caspase-12 at 48 hours. Similarly, EGCG treatment for 30 days effectively recovered compliance and intercontractile interval, submucosal ER stress-related apoptosis (CHOP and caspase-12) at 30 days after pBOO. CONCLUSIONS EGCG alleviate pBOO-induced bladder injury and dysfunction via suppression of inflammation and ER stress-related apoptosis. (C) 2016 Elsevier Inc.
引用
收藏
页码:242.e1 / 242.e9
页数:9
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