Table of Contents Author Guidelines Submit a Manuscript
Oxidative Medicine and Cellular Longevity
Volume 2015 (2015), Article ID 906787, 8 pages
Research Article

Allopurinol Protects against Ischemia/Reperfusion-Induced Injury in Rat Urinary Bladders

1Department of Urology, School of Medicine, Chungnam National University Hospital, Daejeon 301-721, Republic of Korea
2Department of Surgery, School of Medicine, Chungnam National University Hospital, Daejeon 301-721, Republic of Korea
3Division of Bioconvergence Analysis, Korea Basic Science Institute (KBSI), Daejeon 305-333, Republic of Korea
4Department of Functional Genomics, University of Science and Technology (UST), Daejeon 305-806, Republic of Korea

Received 18 December 2014; Revised 27 February 2015; Accepted 19 March 2015

Academic Editor: Aldrin V. Gomes

Copyright © 2015 Ju-Hyun Shin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Bladder ischemia-reperfusion (I/R) injury results in the generation of reactive oxygen species (ROS) and markedly elevates the risk of lower urinary tract symptoms (LUTS). Allopurinol is an inhibitor of xanthine oxidase (XO) and thus can serve as an antioxidant that reduces oxidative stress. Here, a rat model was used to assess the ability of allopurinol treatment to ameliorate the deleterious effects of urinary bladder I/R injury. I/R injury reduced the in vitro contractile responses of longitudinal bladder strips, elevated XO activity in the plasma and bladder tissue, increased the bladder levels of tumor necrosis factor-α (TNF-α), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase, reduced the bladder levels of extracellular regulated kinase (ERK), and decreased and increased the bladder levels of Bcl-2 and Bax, respectively. I/R injury also elevated lipid peroxidation in the bladder. Allopurinol treatment in the I/R injury was generated significantly ameliorating all I/R-induced changes. Moreover, an in situ fluorohistological approach also showed that allopurinol reduces the generation of intracellular superoxides enlarged by I/R injury. Together, the beneficial effects of allopurinol reducing ROS production may be mediated by normalizing the activity of the ERK, JNK, and Bax/Bcl-2 pathways and by controlling TNF-α expression.