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Inflammation. 2014 Aug;37(4):1307-16. doi: 10.1007/s10753-014-9858-5.

Anti-inflammatory effects of triptolide in LPS-induced acute lung injury in mice.

Author information

1
College of Veterinary Medicine, Hebei North University, South Diamond Road, Gaoxin District, 075000, Zhangjiakou, People's Republic of China, hbzjkwd@sina.com.

Abstract

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.

PMID:
24706025
DOI:
10.1007/s10753-014-9858-5
[Indexed for MEDLINE]

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