A Role for Palmitoleate in Regulating Macrophage Activation Conference Paper uri icon


  • Increased macrophage proinflammatory activation contributes to atherosclerotic problems. We investigated the effects of palmitoleate treatment on the inflammatory status of bone marrowderived macrophages (BMDM). After differentiation, wildtype BMDM were treated with palmitoleate (50 M) for 48 h in the presence of lipopolysaccharides (LPS, 100 ng/ml) for the last 30 min to stimulate macrophage proinflammatory signaling or interleukin4 (IL4, 10 ng/ml) for 48 h to inhibit macrophage proinflammatory activation. LPS stimulation caused an increase in the phosphorylation of JNK1/2 and NFB p65 in BMDM. This stimulatory effect of LPS was partially blunted by treatment with palmitoleate. On the other hand, IL4 displayed a weak effect on decreasing the phosphorylation of JNK1/2 and NFB p65 in BMDM. However, in palmitoleatetreated BMDM, the inhibitory effect of IL4 was much more potent, evidenced by the fact that the combined treatment with IL4 and palmitoleate nearly abolished the phosphorylation of JNK1/2 and significantly decreased the phosphorylation of NFB p65. Together, these data suggest that palmitoleate is antiinflammatory bioactive lipid which may be useful for prevention of cardiovascular disease.Grant Funding Source: American Diabetes Association, American Heart Association

published proceedings


author list (cited authors)

  • Xu, H., Guo, X., Li, H., Woo, S., & Wu, C.

citation count

  • 0

complete list of authors

  • Xu, Hang||Guo, Xin||Li, Honggui||Woo, Shih-lung||Wu, Chaodong

publication date

  • April 2013