Triptolide is one of the main active components of Chinese herb Tripterygium wilfordii Hook F, which has been demonstrated to have anti-inflammatory properties. The aim of this study was to investigate the effects of
triptolide on lipopolysaccharide (LPS)-induced
acute lung injury (ALI) in mice and to clarify the possible mechanisms. Mice were administered intranasally with LPS to induce
lung injury.
Triptolide was administered intraperitoneally 1 h before LPS challenge.
Triptolide-treated mice exhibited significantly reduced leukocyte,
myeloperoxidase (MPO) activity,
edema of the lung, as well as TNF-α, IL-1β, and
IL-6 production in the bronchoalveolar lavage fluid compared with LPS-treated mice. Additionally, Western blot analysis showed that
triptolide inhibited the phosphorylation of inhibitor-kappa B
kinase-alpha (IκB-α), p65,
nuclear factor kappa B (NF-κB), p38, extracellular receptor
kinase (ERK), and Jun N-terminal
kinase (JNK) and the expression of
Toll-like receptor 4 (TLR4) caused by LPS. In conclusion, our results suggested that the promising anti-inflammatory mechanism of
triptolide may be that
triptolide activates peroxisome proliferation-activated receptor gamma (
PPAR-γ), thereby attenuating an LPS-induced inflammatory response.
Triptolide may be a promising potential therapeutic reagent for ALI treatment.