期刊
INFLAMMATION
卷 37, 期 4, 页码 1307-1316出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-014-9858-5
关键词
triptolide; lipopolysaccharide (LPS); acute lung injury (ALI); MAPKs; nuclear factor kappa B (NF-kappa B); TLR4
资金
- Science and Technology Pillar Program of Hebei Province, China [13227110D]
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-alpha, IL-1 beta, 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 (I kappa B-alpha), p65, nuclear factor kappa B (NF-kappa B), 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-gamma), thereby attenuating an LPS-induced inflammatory response. Triptolide may be a promising potential therapeutic reagent for ALI treatment.
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