期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 54, 期 -, 页码 12-23出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2017.10.019
关键词
Cirrhosis; CCl4; Hepatotoxicity; Hepaprotective molecule; Liver immune response; Inflammation; Anti-inflammatory response; Liver immune response; Inflammation
资金
- ICyTDF project [312/2009]
- DGAPA-UNAM project [IN225909]
- CONACyT (Rebeca Perez Cabeza de Vaca CVU) [298432]
- PAEP-UNAM
Cirrhosis is a liver pathology originated by hepatocytes, Kupffer and hepatic stellate cells interactions and transformations. This pathology is associated with inflammation and fibrosis, originated by molecular signals secreted by immunological and parenchymal cells, such as cytokines and chemokines, like IL-1 beta, IL-6, TNF-alpha or MCP-1, driven by Kupffer cells signals. As part of inflammation resolution, the same activated Kupffer cells contribute to anti-inflammatory effects with IL-10 and MMP-9 secretion. In a Wistar rat model, cirrhosis induced with CCl4 is characterized by increased inflammatory cytokines, IL-6, IL-1 beta, MCP-1, and TNF-alpha, in plasma and liver tissue. The IFC-305 compound, an adenosine derivative salt, reverses the cirrhosis in this model, suggesting that immune mechanisms related to inflammation should be explored. The IFC-305 reduced inflammatory cytokines, supporting the anti-inflammatory effects induced by the elevation of IL-10, as well as the reduction of M1 inflammatory macrophages (CD11b/c(+)/CD163(+)) and the increase of M2 anti-inflammatory macrophages (HIS36(/)(+)CD11b(+)), measured by flow cytometry. Furthermore, the IFC-305 enhances the metabolic activity of arginase and moderates the inducible nitric oxide synthetase, evaluated through biochemical and immunohistochemical methods. These results contribute to understand the function of the IFC-305, which modulates the immune response in the Wistar rat model of CCl4-induced cirrhosis and support the hepatic protective action through an anti-inflammatory effect, mainly mediated by Kupffer cells.
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