The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.
Allopurinol inhibits CXC chemokine expression and leukocyte adhesion in endotoxemic liver injury.
OBJECTIVE: Leukocyte activation and recruitment are rate limiting steps in endotoxemic liver injury. We investigated the effect of allopurinol on the expression of CXC chemokines and leukocyte-endothelium interactions, microvascular perfusion failure, and cellular injury and apoptosis in endotoxemic liver injury. MATERIALS AND METHODS: Mice were treated with allopurinol prior to challenge with lipopolysaccharide (LPS) + D-Galactosamine (Gal). Intravital microscopy of the liver microcirculation and analysis of liver enzymes were conducted 6 h later. RESULTS: We observed that allopurinol pre-treatment reduced the number of firmly adherent leukocytes by more than 57% in postsinusoidal venules of endotoxemic mice. Indeed, endotoxin-induced liver injury enzymes were decreased by 76% and sinusoidal perfusion failure was reversed in mice pre-treated with allopurinol. Moreover, administration of allopurinol reduced LPS-induced hepatocyte apoptosis by 56%. Notably, it was found that allopurinol significantly decreased the levels of CXC chemokines (more than 83% reduction) in livers of endotoxemic mice. CONCLUSIONS: This study shows that allopurinol markedly protects against endotoxemic liver injury and indicates that reactive oxygen species (ROS) mediate synthesis of CXC chemokines and leukocyte adhesion in the liver in vivo.[1]References
- Allopurinol inhibits CXC chemokine expression and leukocyte adhesion in endotoxemic liver injury. Xiang, L., Klintman, D., Thorlacius, H. Inflamm. Res. (2003) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Use
