| First Author | Wu J | Year | 2011 |
| Journal | Biochem Biophys Res Commun | Volume | 408 |
| Issue | 3 | Pages | 382-7 |
| PubMed ID | 21501589 | Mgi Jnum | J:172053 |
| Mgi Id | MGI:5003374 | Doi | 10.1016/j.bbrc.2011.04.013 |
| Citation | Wu J, et al. (2011) Lipoxin A(4) inhibits the production of proinflammatory cytokines induced by beta-amyloid in vitro and in vivo. Biochem Biophys Res Commun 408(3):382-7 |
| abstractText | Studies increasingly indicate that inflammation induced by beta-amyloid (Abeta) contributes to the progression of Alzheimer's disease (AD). How to inhibit the enhanced production of proinflammatory cytokines stimulated by Abeta is an important research subject for the treatment of AD. In this study, we investigated the inhibitory effect and the molecular mechanism of the lipoxin A(4) (LXA(4)) on the production of interleukin-1beta (IL-1beta) and tumor necrosis factoralpha (TNFalpha) induced by beta-amyloid in the cortex and hippocampus of mice, and in Abeta-stimulated BV2 cells, a mouse microglial cell line. LXA(4) down-regulated the protein expression of IL-1beta and TNFalpha, attenuated the gene expressions of IL-1beta and TNFalpha, inhibited the degradation of IkappaBalpha, inhibited translocation of NF-kappaB p65 subunit into the nucleus induced by beta-amyloid in the cortex and hippocampus of mice, and in Abeta-stimulated BV2 cells, and the inhibitory effects were dose dependently elevated. Our findings suggest that LXA(4) inhibits the production of IL-1beta and TNFalpha induced by beta-amyloid in the cortex and hippocampus of mice, and in BV2 microglial cells via the NF-kappaB signal pathway. |
