| First Author | Souza CO | Year | 2017 |
| Journal | Clin Exp Pharmacol Physiol | Volume | 44 |
| Issue | 5 | Pages | 566-575 |
| PubMed ID | 28135761 | Mgi Jnum | J:360228 |
| Mgi Id | MGI:7797548 | Doi | 10.1111/1440-1681.12736 |
| Citation | Souza CO, et al. (2017) Palmitoleic acid reduces the inflammation in LPS-stimulated macrophages by inhibition of NFkappaB, independently of PPARs. Clin Exp Pharmacol Physiol 44(5):566-575 |
| abstractText | Palmitoleic acid (PM, 16:1n-7) has anti-inflammatory properties that could be linked to higher expression of PPARalpha, an inhibitor of NFkappaB. Macrophages play a major role in the pathogenesis of chronic inflammation, however, the effects of PM on macrophages are underexplored. Thus, we aimed to investigate the effects of PM in activated macrophages as well the role of PPARalpha. Primary macrophages were isolated from C57BL/6 wild type (WT) and PPARalpha knockout (KO) mice, cultured under standard conditions and exposed to lipopolysaccharides LPS (2.5 mug/ml) and PM 600 mumol/L conjugated with albumin for 24 hours. The stimulation with LPS increased the production of interleukin (IL)-6 and IL-1beta while PM decreased the production of IL-6 in WT macrophages. In KO macrophages, LPS increased the production of tumour necrosis factor (TNF)-alpha and IL-6 and PM decreased the production of TNFalpha. The expression of inflammatory markers such NFkappaB and IL1beta were increased by LPS and decreased by PM in both WT and KO macrophages. PM reduced the expression of MyD88 and caspase-1 in KO macrophages, and the expression of TLR4 and HIF-1alpha in both WT and KO macrophages, although LPS had no effect. CD86, an inflammatory macrophage marker, was reduced by PM independently of genotype. PM increased PPARgamma and reduced PPARbeta gene expression in macrophages of both genotypes, and increased ACOX-1 expression in KO macrophages. In conclusion, PM promotes anti-inflammatory effects in macrophages exposed to LPS through inhibition of inflammasome pathway, which was independent of PPARalpha, PPARUpsilon and AMPK, thus the molecular mechanisms of anti-inflammatory response caused by PM is still unclear. |
