Epigallocatechin Gallate Attenuates Partial Bladder Outlet Obstruction-induced Bladder Injury via Suppression of Endoplasmic Reticulum Stress-related Apoptosis‿span style='font-style: italic'>In Vivo Study

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• 作者：Ju-Ton Hsieh^a ; Kuan-Lin Kuo^a ; ^b ; Shing-Hwa Liu^b ; Chung-Sheng Shi^c ; ^d ; Hong-Chiang Chang^a ; Wei-Chou Lin^e ; Chien-Tso Chou^a ; Chen-Hsun Hsu^a ; Shih-Ming Liao^a ; Zuo-He Wang^a ; Chih-Chien Li^a ; Kuo-How Huang^a ; ^{khhuang123@ntu.edu.tw" class="auth_mail" title="E-mail the corresponding author}
• 刊名：Urology
• 出版年：2016
• 出版时间：May 2016
• 年：2016
• 卷：91
• 期：Complete
• 页码：242.e1-242.e9
• 全文大小：2043 K

文摘

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.