ArticleOxidative medicine and cellular longevity2015
Allopurinol Protects against Ischemia/Reperfusion-Induced Injury in Rat Urinary Bladders.
Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- The Dual Role of Interleukin-6 in the Pathophysiology of Skeletal Muscle: Mechanisms, Challenges, and Therapeutic Prospects.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Serendipitous Symptom Control: Allopurinol for Spasticity in a Case of SPG4-Linked Hereditary Spastic Paraplegia-A Case Report.Clinical case reports · 2026Article
- Mediating Effect of Serum Uric Acid in the Association Between Nocturia and Mortality.International neurourology journal · 2025Article
- Mechanism of xanthine oxidase in flap ischemia-reperfusion injury and advances in targeted therapy: a mini review.Frontiers in physiology · 2025Review
- Expression of bladder αInvestigative and clinical urology · 2020Article
- Regulation of Chemokine Function: The Roles of GAG-Binding and Post-Translational Nitration.International journal of molecular sciences · 2017Review
- Renalase as a Novel Biomarker for Evaluating the Severity of Hepatic Ischemia-Reperfusion Injury.Oxidative medicine and cellular longevity · 2016Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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