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
Department of Urology, National Taiwan University Hospital and College of Medicine, National Taiwan University, Taipei, Taiwan.
Department of Urology, National Taiwan University Hospital and College of Medicine, National Taiwan University, Taipei, Taiwan; Graduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Urology. 2016 May;91:242.e1-9. doi: 10.1016/j.urology.2015.12.020. Epub 2016 Jan 25.
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.
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.
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.
EGCG alleviate pBOO-induced bladder injury and dysfunction via suppression of inflammation and ER stress-related apoptosis.
研究绿茶提取物表没食子儿茶素没食子酸酯（EGCG）对大鼠部分膀胱出口梗阻（pBOO）所致膀胱损伤的保护作用。
雌性Sprague-Dawley大鼠接受假手术或膀胱出口梗阻手术，并分为几组（生理盐水注射假手术组、EGCG治疗假手术组、生理盐水注射膀胱出口梗阻组、EGCG治疗膀胱出口梗阻组）。每组大鼠随机分为2组（膀胱出口梗阻手术后48小时和30天），以便在这两个时间点采集膀胱。在研究期间，膀胱出口梗阻手术后通过腹腔注射给予EGCG（4.5毫克/千克/天）和生理盐水。通过蛋白质免疫印迹法和组织学染色检查膀胱组织的炎症、内质网（ER）应激相关凋亡标志物。
膀胱出口梗阻48小时后导致急性膀胱损伤（出血、水肿和中性粒细胞浸润）。此外，膀胱测压显示排尿压力和收缩间期降低。我们还观察到在48小时时环氧合酶-2、聚（ADP-核糖）聚合酶的表达增加，以及内质网应激标志物如半胱天冬酶-12和CCAAT/增强子结合蛋白同源蛋白（CHOP）的表达增加。EGCG治疗显著改善了膀胱出口梗阻所致的组织学变化、膀胱功能障碍以及48小时时环氧合酶-2、CHOP和半胱天冬酶-12的过度表达。同样，EGCG治疗30天有效恢复了膀胱出口梗阻30天后的顺应性和收缩间期、黏膜下内质网应激相关凋亡（CHOP和半胱天冬酶-12）。
EGCG通过抑制炎症和内质网应激相关凋亡减轻膀胱出口梗阻所致的膀胱损伤和功能障碍。
