| First Author | Li Y | Year | 2008 |
| Journal | Eur J Pharmacol | Volume | 590 |
| Issue | 1-3 | Pages | 417-22 |
| PubMed ID | 18593575 | Mgi Jnum | J:138290 |
| Mgi Id | MGI:3804753 | Doi | 10.1016/j.ejphar.2008.06.047 |
| Citation | Li Y, et al. (2008) Human ApoA-I overexpression diminishes LPS-induced systemic inflammation and multiple organ damage in mice. Eur J Pharmacol 590(1-3):417-22 |
| abstractText | 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. |
