title: The preventative role of curcumin on the lung inflammatory response induced by cardiopulmonary bypass in rats.
abstract: BACKGROUND
  Acute lung injury is a frequent complication after cardiopulmonary bypass (CPB). Recent studies have reported that NF-κB plays an important role in the pathogenesis of post-CPB pulmonary dysfunction. Several signaling pathways, including the TLR4 pathway, induce NF-κB leading to an inflammatory response. We designed this study to determine whether or not curcumin inhibits TLR4 and MyD88 protein levels and ameliorates lung inflammatory injury in a rat CPB model.
  
  
  METHODS
  Sprague-Dawley rats were randomly divided into the following five groups (n = 12): sham; control (CPB); vehicle; low-dose curcumin (L-Cur); and high-dose curcumin (H-Cur). The percutaneous beating heart CPB model of rat was established. Animals were pretreated with a single intraperitoneal injection of vehicle, L-Cur (50 mg/kg), or H-Cur (200 mg/kg) 2 h prior to CPB. Blood were sampled at various time points, then lung tissues and bronchoalveolar lavage fluid were harvested 24 h after CPB.
  
  
  RESULTS
  CPB induced a marked increase in the concentrations of interleukin-8, tumor necrosis factor-α, and matrix metalloproteinase-9 in plasma, bronchoalveolar lavage fluid, and lung tissues (P < 0.05 versus sham group), whereas curcumin pretreatment reduced these inflammatory markers. Curcumin had effective inhibitory effects on the expression of TLR4, MyD88, and NF-κB in lung tissues 24 h post-CPB (P < 0.05 versus vehicle group). Administration of curcumin remarkably decreased the lung injury score (L-Cur versus vehicle group, P = 0.024; H-Cur versus vehicle group, P = 0.013).
  
  
  CONCLUSIONS
  Curcumin may be an alternative therapy for protecting CPB-induced lung injury by suppressing the expression of inflammatory cytokines. This anti-inflammatory effect of curcumin is partly related to the inhibition of TLR4, MyD88, and NF-κB.
authors.affiliation: Department of Cardiothoracic Surgery, Jinling Hospital, Clinical Medicine School of Nanjing University, Nanjing, China.
authors.forename: Kun
authors.initials: K
authors.lastname: Liu
authors.forename: Li
authors.initials: L
authors.lastname: Shen
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Guohua
authors.initials: G
authors.lastname: Dong
authors.forename: Haiwei
authors.initials: H
authors.lastname: Wu
authors.forename: Hongtao
authors.initials: H
authors.lastname: Shao
authors.forename: Hua
authors.initials: H
authors.lastname: Jing
mesh_terms: D000818:Animals; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D003474:Curcumin / Q000494:pharmacology*; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000097:blood; D053594:Myeloid Differentiation Factor 88 / Q000032:analysis / Q000037:antagonists & inhibitors; D016328:NF-kappa B / Q000032:analysis / Q000037:antagonists & inhibitors; D011014:Pneumonia / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D051197:Toll-Like Receptor 4 / Q000032:analysis / Q000037:antagonists & inhibitors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D016209:Interleukin-8; C507781:Myd88 protein, rat; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; C495347:Tlr4 protein, rat; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D020780:Matrix Metalloproteinase 9; D003474:Curcumin