title: Paeoniflorin protects against lipopolysaccharide-induced acute lung injury in mice by alleviating inflammatory cell infiltration and microvascular permeability.
abstract: OBJECTIVE
  The present study aims to explore the effects of paeoniflorin (PF), a monoterpene glycoside isolated from the roots of Paeonia lactiflora Pallas, on acute lung injury (ALI) and the possible mechanisms.
  
  
  METHODS
  ALI was induced in mice by an intratracheal instillation of lipopolysaccharide (LPS, 1 mg/kg), and PF was injected intraperitoneally 30 min prior to LPS administration. After 24 h, lung water content, histology, microvascular permeability and proinflammatory cytokines in the bronchoaveolar lavage fluid were evaluated.
  
  
  RESULTS
  It was shown that PF (50, 100 mg/kg) could alleviate LPS-induced ALI, evidenced by reduced pulmonary edema, improved histological changes, and attenuated inflammatory cell accumulation in the interstitium and alveolar space as well as microvascular permeability. It also markedly down-regulated the expressions of proinflammatory cytokines interleukin (IL)-1β and tumor necrosis factor (TNF)-α at both transcription and protein levels. Additionally, PF inhibited the phosphorylations of p38 MAP kinase (p38) and c-Jun NH2-terminal kinase (JNK) but not extracellular signal-regulated kinase (ERK), and prevented the activation of nuclear factor-kappa B (NF-κB) in the lung tissues.
  
  
  CONCLUSIONS
  The findings suggest that PF is able to alleviate ALI, and the underlying mechanisms are probably attributed to decreasing the production of proinflammatory cytokines through down-regulation of the activation of p38, JNK and NF-κB pathways in lung tissues.
authors: Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing 210009, China.
authors: Haiqiang
authors: H
authors: Zhou
authors: Difei
authors: D
authors: Bian
authors: Xiaolan
authors: X
authors: Jiao
authors: Zhifeng
authors: Z
authors: Wei
authors: Haofang
authors: H
authors: Zhang
authors: Yufeng
authors: Y
authors: Xia
authors: Yisheng
authors: Y
authors: He
authors: Yue
authors: Y
authors: Dai
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001565:Benzoates / Q000494:pharmacology*; D001952:Bridged-Ring Compounds / Q000494:pharmacology*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005960:Glucosides / Q000494:pharmacology*; D007249:Inflammation; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism*; D055370:Lung Injury / Q000473:pathology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D008833:Microcirculation; D039821:Monoterpenes; D016328:NF-kappa B / Q000378:metabolism; D010539:Permeability; D010766:Phosphorylation; D011654:Pulmonary Edema / Q000473:pathology; D015398:Signal Transduction; D013997:Time Factors; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism; D006027:Glycosides
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001565:Benzoates; D001952:Bridged-Ring Compounds; D048049:Extracellular Signal-Regulated MAP Kinases; D005960:Glucosides; D048031:JNK Mitogen-Activated Protein Kinases; D008070:Lipopolysaccharides; D039821:Monoterpenes; D016328:NF-kappa B; D048051:p38 Mitogen-Activated Protein Kinases; C015423:peoniflorin; D006027:Glycosides