Anti-inflammatory effects of triptolide in LPS-induced acute lung injury in mice.
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.
College of Veterinary Medicine, Hebei North University, South Diamond Road, Gaoxin District, 075000, Zhangjiakou, People's Republic of China, hbzjkwd@sina.com.
Dong
D
Wei
Zhihong
Z
Huang
D055371:Acute Lung Injury / Q000188:drug therapy*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D004224:Diterpenes / Q000494:pharmacology*; D004852:Epoxy Compounds / Q000494:pharmacology; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007962:Leukocytes / Q000166:cytology; D008024:Ligands; D008070:Lipopolysaccharides / Q000737:chemistry*; D020935:MAP Kinase Signaling System; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000378:metabolism; D047495:PPAR gamma / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D010616:Phenanthrenes / Q000494:pharmacology*; D010936:Plant Extracts / Q000737:chemistry; D029757:Tripterygium / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D004224:Diterpenes; D004852:Epoxy Compounds; D053583:Interleukin-1beta; D015850:Interleukin-6; D008024:Ligands; D008070:Lipopolysaccharides; D016328:NF-kappa B; D047495:PPAR gamma; D010616:Phenanthrenes; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; C001899:triptolide; D009195:Peroxidase