Secondary Logo

Institutional members access full text with Ovid®

Neuroprotection of green tea catechins on surgical menopause-induced overactive bladder in a rat model

Juan, Yung-Shun MD1,2,3; Chuang, Shu-Mien PhD4; Long, Cheng-Yu MD, PhD5,6; Chen, Chung-Hwan MD7; Levin, Robert M. PhD8; Liu, Keh-Min PhD4; Huang, Chun-Hsiung MD, PhD2,3

Menopause: The Journal of The North American Menopause Society: March 2012 - Volume 19 - Issue 3 - p 346–354
doi: 10.1097/gme.0b013e31822d652d
Original Articles
Buy

Objective A rat model of ovariectomy-induced voiding dysfunction has been established, which mimicked the urge incontinence in postmenopausal women. Previous studies have identified strong anti-inflammatory/antioxidant properties of green tea and its associated polyphenols. The aim of this study was to evaluate whether the green tea extract, epigallocatechin gallate (EGCG), could prevent an ovariectomy-induced overactive bladder.

Methods The study included 48 female Sprague-Dawley rats, which were divided into four groups. After bilateral ovariectomy during the following 6-month period, 12 rats received an intraperitoneal injection of saline, 24 rats received either a low-dose (1 μM kg−1 d−1) or a high-dose (10 μM kg−1 d−1) EGCG intraperitoneal injection. The sham group consisted of twelve rats that were not ovariectomized. In vivo isovolumetric cystometrograms were performed in all groups before the animals were euthanized. The immunofluorescence study used neurofilament stains to evaluate intramural nerve damage. Western immunoblots and real-time polymerase chain reaction were performed to determine M2 and M3 muscarinic cholinergic receptors (MChRs) at both protein and messenger RNA (mRNA) expressions.

Results Long-term ovariectomy significantly increased non–voiding contractions, whereas treatment with EGCG significantly attenuated the frequency of non–voiding contractions. Ovariectomy significantly decreased the numbers of neurofilament and increased M2 and M3 MChR protein and mRNA expressions. Treatment with EGCG restored the amount of neurofilament staining and decreased M2 and M3 MChR protein and mRNA overexpressions.

Conclusions This study confirmed that ovary hormone deficiency induced overactive bladder dysfunction via intramural nerve damage and muscarinic receptor overexpression. EGCG prevented ovariectomy-induced bladder dysfunction through neuroprotective effects in a dose-dependent fashion.

Epigallocatechin gallate prevented ovariectomy-induced bladder dysfunction through neuroprotective effects in a dose-dependent fashion.

From the 1Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; 2Department of Urology, College of Medicine; 3Department of Urology, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; 4Department of Anatomy, College of Medicine; 5Excellence for Environmental Medicine, College of Medicine, Kaohsiung Medical University; 6Department of Obstetrics and Gynecology, Kaohsiung Municipal Hsia-Kang Hospital; 7Department of Orthopedics, Kaohsiung Medical University Hospital; Kaohsiung, Taiwan; and 8Albany College of Pharmacy, Albany, NY.

Received May 24, 2011; revised and accepted July 12, 2011.

Funding/support: This study was supported by grants from Kaohsiung Medical University Hospital (KMUH98-8R07).

Financial disclosure/conflicts of interest: None reported.

Address correspondence to: Chun-Hsiung Huang, MD, PhD, Department of Urology, Kaohsiung Medical University, 100 Shih-Chuan 1st Road, Sanmin District, Kaohsiung City 807, Taiwan. E-mail: chhuang@kmu.edu.tw

©2012The North American Menopause Society