Omega-3 fatty acid intervention suppresses lipopolysaccharide-induced inflammation and weight loss in mice

Mar Drugs. 2015 Feb 13;13(2):1026-36. doi: 10.3390/md13021026.

Abstract

Bacterial endotoxin lipopolysaccharide (LPS)-induced sepsis is a critical medical condition, characterized by a severe systemic inflammation and rapid loss of muscle mass. Preventive and therapeutic strategies for this complex disease are still lacking. Here, we evaluated the effect of omega-3 (n-3) polyunsaturated fatty acid (PUFA) intervention on LPS-challenged mice with respect to inflammation, body weight and the expression of Toll-like receptor 4 (TLR4) pathway components. LPS administration induced a dramatic loss of body weight within two days. Treatment with n-3 PUFA not only stopped loss of body weight but also gradually reversed it back to baseline levels within one week. Accordingly, the animals treated with n-3 PUFA exhibited markedly lower levels of inflammatory cytokines or markers in plasma and tissues, as well as down-regulation of TLR4 pathway components compared to animals without n-3 PUFA treatment or those treated with omega-6 PUFA. Our data demonstrate that n-3 PUFA intervention can suppress LPS-induced inflammation and weight loss via, at least in part, down-regulation of pro-inflammatory targets of the TLR4 signaling pathway, and highlight the therapeutic potential of n-3 PUFA in the management of sepsis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Cytokines / blood
  • Fatty Acids, Omega-3 / pharmacology*
  • Gene Expression / drug effects
  • Inflammation / chemically induced
  • Inflammation / prevention & control*
  • Lipopolysaccharides / antagonists & inhibitors*
  • Lipopolysaccharides / toxicity
  • Mice
  • Toll-Like Receptor 4 / biosynthesis
  • Weight Loss / drug effects*

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Cytokines
  • Fatty Acids, Omega-3
  • Lipopolysaccharides
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4