• Users Online: 107
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
Year : 2019  |  Volume : 5  |  Issue : 2  |  Page : 55-61

Uric acid therapy for vasculoprotection in acute ischemic stroke

1 Comprehensive Stroke Center, Hospital Clínic, University of Barcelona; Department of Neuroscience, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Universitat Autònoma de Barcelona, Barcelona, Spain
2 Department de Farmacologia, de Terapèutica i de Toxicologia, Facultat de Medicina, Universitat Autònoma de Barcelona, Barcelona, Spain

Correspondence Address:
Prof. ┴ngel Chamorro
Hospital Clinic of Barcelona, Villarroel 170, 08036 Barcelona
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/bc.bc_1_19

Rights and Permissions

Uric acid (UA) is a product of the catabolism of purine nucleotides, the principal constituents of DNA, RNA, and cellular energy stores, such as adenosine triphosphate. The main properties of UA include scavenging of hydroxyl radicals, superoxide anion, hydrogen peroxide, and peroxynitrite that make this compound to be the most potent antioxidant in the human plasma. As the result of two silencing mutations in the gene of the hepatic enzyme uricase which degrades UA to allantoin, humans have higher levels of UA than most mammals. However, these levels rapidly decrease following an acute ischemic stroke (AIS), and this decrement has been associated to worse stroke outcomes. This review highlights the safety and potential clinical value of UA therapy in AIS, particularly in patients more exposed to redox-mediated mechanism following the onset of ischemia, such as women, hyperglycemic patients, or patients treated with mechanical thrombectomy. The clinical findings are supported by preclinical data gathered in different laboratories, and in assorted animal species which include male and female individuals or animals harboring comorbidities frequently encountered in patients with AIS, such as hyperglycemia or hypertension. A remarkable finding in these studies is that UA targets its main effects in the brain vasculature since available evidence suggests that does not seem to cross the blood–brain barrier. Altogether, the available data with UA therapy extend the importance of vasculoprotection for effective neuroprotection at the bedside and reinforce the role of endothelial cells after brain ischemia for an increased survival of the whole neurovascular unit.

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded324    
    Comments [Add]    
    Cited by others 12    

Recommend this journal