Heparin attenuates lipopolysaccharide-induced acute lung injury by inhibiting nitric oxide synthase and transforming growth factor - β/Smad signaling pathway

Chinese Critical Care Medicine

Volumn 26, Issue 11, 2014, Pages 810-814

  Mu, En ^a   Ding, Renyu ^c   An, Xin ^c   Li, Xin ^c   Chen, Song ^c   Ma, Xiaochun ^b  

^a Tianjin Hospital   (China)

^b CHINA MEDICAL UNIVERSITY   (China)

^c NONE

Author keywords

Acute lung injury; Acute respiratory distress syndrome; Heparin; Nitric oxide synthase; Transforming growth factor Smad signaling pathway

Indexed keywords

HEPARIN; INDUCIBLE NITRIC OXIDE SYNTHASE; INTERLEUKIN 6; LIPOPOLYSACCHARIDE; MALONALDEHYDE; MESSENGER RNA; MYELOPEROXIDASE; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; SMAD PROTEIN; TRANSFORMING GROWTH FACTOR BETA; TUMOR NECROSIS FACTOR ALPHA; SMAD2 PROTEIN; SMAD3 PROTEIN; TRANSFORMING GROWTH FACTOR BETA1; TUMOR NECROSIS FACTOR;

ACUTE LUNG INJURY; ADULT; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CAPILLARY ENDOTHELIAL CELL; COMPARATIVE STUDY; CONTROLLED STUDY; ENZYME LINKED IMMUNOSORBENT ASSAY; HISTOPATHOLOGY; IMMUNOHISTOCHEMISTRY; LUNG ALVEOLUS; LUNG HEMORRHAGE; LUNG LAVAGE; LUNG PARENCHYMA; NONHUMAN; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; RAT; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; SIGNAL TRANSDUCTION; WESTERN BLOTTING; ANIMAL; CHEMICALLY INDUCED; DRUG EFFECTS; METABOLISM; RANDOMIZATION; SPRAGUE DAWLEY RAT; TREATMENT OUTCOME; BRONCHOALVEOLAR LAVAGE FLUID; CELL INFILTRATION; ENZYME INHIBITION; LIPOPOLYSACCHARIDE-INDUCED ACUTE LUNG INJURY; LUNG ALVEOLUS EPITHELIUM CELL; LUNG FUNCTION TEST; LUNG WET DRY RATIO; PROTEIN FUNCTION; PROTEIN PROTEIN INTERACTION;

ACUTE LUNG INJURY; ANIMALS; BRONCHOALVEOLAR LAVAGE FLUID; HEPARIN; INTERLEUKIN-6; LIPOPOLYSACCHARIDES; NITRIC OXIDE SYNTHASE; PULMONARY ALVEOLI; RANDOM ALLOCATION; RATS; RATS, SPRAGUE-DAWLEY; RNA, MESSENGER; SIGNAL TRANSDUCTION; SMAD PROTEINS; TRANSFORMING GROWTH FACTOR BETA; TREATMENT OUTCOME;

EID: 84912123635     PISSN: 10030603     EISSN: None     Source Type: Journal    
DOI: 10.3760/cma.j.issn.2095-4352.2014.11.009     Document Type: Article

References (14)

1. Ware LB, Matthay MA. The acute respiratory distress syndrome [J]. N Engl J Med,2000,342,(18):1334-1349.
2. Fernandes AB, Zin WA, Rocco PR. Corticosteroids in acute respiratory distress syndrome [J]. Braz J Med Biol Res,2005,38(2):147-159.
3. Matthay MA, Zemans RL. The acute respiratory distress syndrome: pathogenesis and treatment [J]. Annu Rev Pathol,2011,6:147-59.
4. Lever R, Page CP. Novel drug development opportunities for heparin [J]. Nat Rev Drug Discov,2002,1(2):140-148.
5. Murakami K, McGuire R, Cox RA, et al. Heparin nebulization attenuates acute lung injury in sepsis following smoke inhalation in sheep [J]. Shock,2002,18(3):236-241.
6. Ritter C, da Cunha AA, Echer IC, et al. Effects of N-acetylcysteine plus deferoxamine in lipopolysaccharide-induced acute lung injury in the rat [J]. Crit Care Med,2006,34(2):471-477.
7. Wang M, He J, Mei B, et al. Therapeutic effects and anti-inflammatory mechanisms of heparin on acute lung injury in rabbits lung injury in rabbits [J]. Acad Emerg Med,2008,15(7):656-663.
8. Levi M, van der Poll T. Inflammation and coagulation [J]. Crit Care Med,2010,38(2 Suppl):S26-34.
9. Kobayashi A, Hashimoto S, Kooguchi K, et al. Expression of inducible nitric oxide synthase and inflammatory cytokines in alveolar macrophages of ARDS following sepsis [J]. Chest,1998,113,6,1632-1639.
10. Wesselkamper SC, Case LM, Henning LN, et al. Gene expression changes during the development of acute lung injury : role of transforming growth factor beta [J]. Am J Respir Crit Care Med,2005,172(11):1399-1411.
11. Fathy RJ, Lichtenberger F, McKeegan CB, et al. The acute respiratory distress syndrome: a role for transforming growth factor-beta 1 [J]. Am J Respir Cell Mol Biol,2003,28(4):499-503.
12. Derynck R, Zhang Y, Feng XH. Smads : transcriptional activators of TGF-beta responses [J]. Cell,1998,95(6):737-740.
13. Lu Q, Harrington EO, Jackson H, et al. Transforming growth factor-beta1-induced endothelial barrier dysfunction involves Smad2-dependent p38 activation and subsequent RhoA activation [J]. J Appl Physiol (1985),2006,101(2):375-384.
14. Lee JH, Lee H, Joung YK, et al. The use of low molecular weight heparin-pluronic nanogels to impede liver fibrosis by inhibition the TGF-β/Smad signaling pathway [J]. Biomaterials,2011,32(5):1438-1445