Sesamin Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibition of TLR4 Signaling Pathways

Inflammation. 2016 Feb;39(1):467-472. doi: 10.1007/s10753-015-0270-6.


Recent studies suggested that TLR4 signaling pathways played an important role in the development of LPS-induced acute lung injury (ALI). Sesamin, a sesame lignan exacted from sesame seeds, has been shown to exhibit significant anti-inflammatory activity. The purpose of this study was to investigate the anti-inflammatory effects of sesamin on LPS-induced ALI in mice. Mice ALI model was induced by intratracheal instillation of LPS. Sesamin was given 1 h after LPS challenge. Our results showed that sesamin inhibited LPS-induced lung pathological change, edema, and myeloperoxidase (MPO) activity. Sesamin suppressed LPS-induced inflammatory cytokines TNF-α, IL-6, and IL-1β production. Furthermore, sesamin inhibited LPS-induced TLR4 expression and NF-κB activation. In conclusion, the results of this study indicated that sesamin protected against LPS-induced ALI by inhibition of TLR4 signaling pathways.

Keywords: LPS; NF-κB; TLR4; acute lung injury; sesamin.

MeSH terms

  • Acute Lung Injury / drug therapy*
  • Animals
  • Anti-Inflammatory Agents / therapeutic use*
  • Dioxoles / therapeutic use*
  • Edema / drug therapy
  • Edema / prevention & control
  • Enzyme Activation / drug effects
  • Interleukin-1beta / biosynthesis
  • Interleukin-6 / biosynthesis
  • Lignans / therapeutic use*
  • Lipopolysaccharides
  • Lung / pathology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B / metabolism
  • Peroxidase / metabolism
  • Signal Transduction / drug effects
  • Toll-Like Receptor 4 / metabolism*
  • Tumor Necrosis Factor-alpha / biosynthesis


  • Anti-Inflammatory Agents
  • Dioxoles
  • IL1B protein, mouse
  • Interleukin-1beta
  • Interleukin-6
  • Lignans
  • Lipopolysaccharides
  • NF-kappa B
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • Peroxidase
  • sesamin