title: Pre-treatment with Cobra venom factor alleviates acute lung injury induced by intestinal ischemia-reperfusion in rats.
abstract: BACKGROUND
  Previous studies have shown that complement activation is required for intestinal ischemia-reperfusion (IIR)-induced tissue damage. Cobra venom factor (CVF), a structural and functional homolog to the activated form of C3 (the central component of the complement system), can cause exhaustive activation of the alternative pathway and deplete the complement components.
  
  
  OBJECTIVE
  This study aims to investigate the effect of CVF pretreatment on acute lung injury induced by IIR in rats.
  
  
  METHODS
  Lung injury was induced by clamping superior mesenteric artery (SMA) for 60 min followed by 4 h of reperfusion. CVF was given via the tail vein 24 h before the operation.
  
  
  RESULTS
  Histological results as well as lung edema determination and permeability assay showed the severe damages were induced in the lungs of rats in the IIR group, accompanying with the increases in the levels of pulmonary malondialdehyde (MDA), myeloperoxidase (MPO) activity, intercellular adhesion molecule-1 (ICAM-1), interleukin (IL)-8. Remarkably, CVF pretreatment significantly attenuated the morphological lung injury, lung edema and lung permeability, reduced the increase of the levels of MDA, MPO, ICAM-1 and IL-8 induced by IIR. In addition, the severe damage of intestinal and elevation of plasma diamine oxidase activity in the IIR rats were significantly alleviated by CVF pretreatment.
  
  
  CONCLUSIONS
  CVF pretreatment could significantly reduce the acute lung injury induced by IIR. The mechanism might include, at least in part, the inhibition of oxidant generation, infiltration of neutrophils, ICAM-1 expression and IL-8 release. CVF might be an efficient reagent for preventing the IIR injuries in clinical condition.
authors.affiliation: Department of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China. jianglaimz@126.com  
authors.forename: Y F
authors.initials: YF
authors.lastname: Mao
authors.forename: Q H
authors.initials: QH
authors.lastname: Yu
authors.forename: X F
authors.initials: XF
authors.lastname: Zheng
authors.forename: K
authors.initials: K
authors.lastname: Liu
authors.forename: W Q
authors.initials: WQ
authors.lastname: Liang
authors.forename: Y W
authors.initials: YW
authors.lastname: Wang
authors.forename: X M
authors.initials: XM
authors.lastname: Deng
authors.forename: L
authors.initials: L
authors.lastname: Jiang
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology / Q000517:prevention & control*; D000818:Animals; D051056:Complement Inactivating Agents / Q000494:pharmacology*; D004546:Elapid Venoms / Q000494:pharmacology*; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics; D016209:Interleukin-8 / Q000378:metabolism; D007421:Intestine, Small / Q000098:blood supply / Q000473:pathology; D008297:Male; D008638:Mesenteric Arteries; D020556:Neutrophil Infiltration / Q000187:drug effects; D016877:Oxidants / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D051056:Complement Inactivating Agents; D004546:Elapid Venoms; D016209:Interleukin-8; D016877:Oxidants; C016310:cobra venom factor; D018799:Intercellular Adhesion Molecule-1