Anti-inflammatory effects of triptolide by inhibiting the NF-κB signalling pathway in LPS-induced acute lung injury in a murine model.
Triptolide is one of the main active components in the Chinese herb Tripterygium wilfordii Hook F, which has been demonstrated to possess 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 explore the possible mechanisms. Mice were administered LPS intranasally to induce lung injury, and triptolide was administered intraperitoneally 1 h prior to the LPS challenge. Triptolide‑treated mice exhibited significantly reduced levels of leukocytes, myeloperoxidase activity and edema of the lung, as well as tumour necrosis factor‑α, interleukin (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 LPS‑induced phosphorylation of nuclear factor of κ light polypeptide gene enhancer in B cells inhibitor‑α and nuclear factor κ‑light‑chain‑enhancer of activated B cells‑p65 (NF‑κB p65) and the expression of Toll‑like receptor 4 (TLR4). In conclusion, the results from the present study suggest that the anti‑inflammatory effect of triptolide against LPS‑induced ALI may be due to its ability to inhibit the TLR4‑mediated NF‑κB signalling pathway. Triptolide may therefore be a promising potential therapeutic agent for ALI treatment, which may ultimately aid the clinical therapy for patients with ALI.
Department of Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430000, P.R. China.
Xian
X
Wang
Department of Clinical Laboratory, The First Affiliated Hospital, College of Medicine, Shihezi University, Shihezi, Xinjiang 832000, P.R. China.
Lei
L
Zhang
Department of Clinical Laboratory, The First Affiliated Hospital, College of Medicine, Shihezi University, Shihezi, Xinjiang 832000, P.R. China.
Wei
W
Duan
Department of Emergency, The First Affiliated Hospital, College of Medicine, Shihezi University, Shihezi, Xinjiang 832000, P.R. China.
Bin
B
Liu
Department of Medical Oncology, The First Affiliated Hospital, College of Medicine, Shihezi University, Shihezi, Xinjiang 832000, P.R. China.
Ping
P
Gong
Department of Public Health, College of Medicine, Shihezi University, Shihezi, Xinjiang 832000, P.R. China.
Yusong
Y
Ding
Department of Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430000, P.R. China.
Xiongwen
X
Wu
D055371:Acute Lung Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001992:Bronchoalveolar Lavage Fluid; D018925:Chemokines / Q000378:metabolism; D004195:Disease Models, Animal; D004224:Diterpenes / Q000494:pharmacology*; D004852:Epoxy Compounds / Q000494:pharmacology; D020672:I-kappa B Proteins / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D010616:Phenanthrenes / Q000494:pharmacology*; D010766:Phosphorylation / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000894:Anti-Inflammatory Agents, Non-Steroidal; D018925:Chemokines; D004224:Diterpenes; D004852:Epoxy Compounds; D020672:I-kappa B Proteins; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D010616:Phenanthrenes; D014409:Tumor Necrosis Factor-alpha; D000072000:NF-KappaB Inhibitor alpha; C001899:triptolide