Platelet-activating factor involvement in thioacetamide-induced experimental liver fibrosis and cirrhosis
Digestive Diseases and Sciences, ISSN: 0163-2116, Vol: 55, Issue: 2, Page: 276-284
2010
- 23Citations
- 19Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations23
- Citation Indexes23
- 23
- CrossRef20
- Captures19
- Readers19
- 19
Article Description
Platelet-activating factor (PAF) is a potent lipid inflammatory mediator acting on cells through its specific receptor. Plasma PAF-acetylhydrolase (PAF-AH) is the main enzyme that inactivates PAF in blood, participating in its homeostasis. The objective of this study was to investigate the involvement of PAF in the liver fibrotic process using an experimental animal model. Liver fibrosis was induced in adult male Wistar rats by administration of thioacetamide (TAA) in drinking water (300 mg/l) for three months. The animals were sacrificed at time 0 (control group) and after 1, 2, and 3 months. PAF levels in liver and blood and PAF-AH activity in plasma were determined. Liver histopathological examination was also performed. TAA administration resulted in progressively increased liver fibrosis, leading finally to the formation of cirrhotic nodules in the liver. Throughout the experiment PAF levels in liver tissue remained stable. "Total" ("free" plus "bound") PAF levels in blood decreased, reaching statistically significant differences in the first and third months compared with the control group (P < 0.05). "Free" PAF levels in blood were higher at one month (P < 0.05) and decreased gradually thereafter. In all treated groups, "bound" PAF levels in blood decreased whereas plasma PAF-AH activity increased (P < 0.05) compared with the control group. Our data indicated alterations of PAF levels in blood and PAF-AH activity during fibrosis induction, implicating participation of PAF in the liver fibrotic process. © 2009 Springer Science+Business Media, LLC.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=76849087846&origin=inward; http://dx.doi.org/10.1007/s10620-009-0745-0; http://www.ncbi.nlm.nih.gov/pubmed/19242794; http://link.springer.com/10.1007/s10620-009-0745-0; https://dx.doi.org/10.1007/s10620-009-0745-0; https://link.springer.com/article/10.1007/s10620-009-0745-0; http://www.springerlink.com/index/10.1007/s10620-009-0745-0; http://www.springerlink.com/index/pdf/10.1007/s10620-009-0745-0
Springer Science and Business Media LLC
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