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Human ApoA-I overexpression diminishes LPS-induced systemic inflammation and multiple organ damage in mice.

Authors: Li, Y  Dong, JB  Wu, MP 
Citation: Li Y, etal., Eur J Pharmacol. 2008 Aug 20;590(1-3):417-22. doi: 10.1016/j.ejphar.2008.06.047. Epub 2008 Jun 16.
Pubmed: (View Article at PubMed) PMID:18593575
DOI: Full-text: DOI:10.1016/j.ejphar.2008.06.047

Apolipoprotein A-I (ApoA-I) is the major apolipoprotein of high density lipoprotein (HDL). To investigate the protective effect of ApoA-I against lipopolysaccharide (LPS)-induced systemic inflammation and multiple organ damage in mice, we established a human ApoA-I overexpression mouse model using recombinant adenovirus vector (AdV-AI). The histomorphologic analysis showed that AdV-AI administration greatly attenuated LPS-induced acute injury in lung and kidney. AdV-AI treatment also significantly inhibited LPS-induced increments of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-1beta levels in serum (P < 0.01, P < 0.05 and P < 0.05, respectively) and in bronchoalverolar lavage fluid (P < 0.05, respectively), and of serum creatine kinase and creatinine levels (P < 0.05, respectively). Moreover, we found that the increments of CD14 expression in liver and lung induced by LPS were significantly reduced by AdV-AI treatment (P < 0.05 and P < 0.01, respectively). In conclusion, adenovirus-mediated ApoA-I overexpression plays a protective effect against LPS-induced systemic inflammation and multiple organ damage in mice. Such effect may attribute partly to the suppression of inflammatory cytokine release and reduction of CD14 expression.

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RGD ID: 7241573
Created: 2013-03-11
Species: All species
Last Modified: 2013-03-11
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.