BML-111, a lipoxin receptor agonist, ameliorates 'two-hit'-induced acute pancreatitis-associated lung injury in mice by the upregulation of heme oxygenase-1

Artificial Cells, Nanomedicine and Biotechnology

Volumn 42, Issue 2, 2014, Pages 110-120

  Wang, Ying Zhen ^a,b   Zhang, You Cheng ^a   Cheng, Jun Sheng ^a   Ni, Qian ^a   Li, Pei Jie ^a   Wang, Shi Wen ^b   Han, Wei ^a   Zhang, Yu Long ^a  

^a LANZHOU UNIVERSITY   (China)

^b Second Hospital of Gansu Province   (China)

Author keywords

Acute pancreatitis associated lung injury; BML 111; Heme oxygenase 1; Severe acute pancreatitis

Indexed keywords

AMYLASES; BODY FLUIDS; ESCHERICHIA COLI; HISTOLOGY; MAMMALS; PORPHYRINS; TISSUE;

ANTI-INFLAMMATORY EFFECTS; BML-111; HEME OXYGENASE-1; INTRAPERITONEAL INJECTIONS; LIPOPOLYSACCHARIDES; LUNG INJURY; POSSIBLE MECHANISMS; SEVERE ACUTE PANCREATITIS;

BIOLOGICAL ORGANS;

AMYLASE; ANTIINFLAMMATORY AGENT; BACTERIUM LIPOPOLYSACCHARIDE; BML 111; CERULETIDE; HEME OXYGENASE 1; INTERLEUKIN 10; INTERLEUKIN 1BETA; LIPOXIN RECEPTOR AGONIST; TUMOR NECROSIS FACTOR ALPHA; UNCLASSIFIED DRUG; 5(S),6(R)-7-TRIHYDROXYHEPTANOIC ACID, METHYL ESTER; CYTOKINE; HEPTANOIC ACID DERIVATIVE; LIPOPOLYSACCHARIDE; LIPOXIN RECEPTOR;

ACUTE PANCREATITIS ASSOCIATED LUNG INJURY; AMYLASE BLOOD LEVEL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIINFLAMMATORY ACTIVITY; ARTICLE; CONTROLLED STUDY; DRUG MECHANISM; HISTOPATHOLOGY; LUNG INJURY; LUNG PARENCHYMA; MOUSE; NONHUMAN; PROTEIN EXPRESSION; RANDOMIZED CONTROLLED TRIAL; UPREGULATION; AGONISTS; ANIMAL; BAGG ALBINO MOUSE; BLOOD; CHEMICALLY INDUCED; COMPLICATION; DISEASE MODEL; DRUG EFFECTS; GENETICS; HUMAN; LUNG; METABOLISM; PANCREAS; PANCREATITIS, ACUTE NECROTIZING; PATHOLOGY;

AMYLASES; ANIMALS; ANTI-INFLAMMATORY AGENTS; CERULETIDE; CYTOKINES; DISEASE MODELS, ANIMAL; HEME OXYGENASE-1; HEPTANOIC ACIDS; HUMANS; LIPOPOLYSACCHARIDES; LUNG; LUNG INJURY; MICE; MICE, INBRED BALB C; PANCREAS; PANCREATITIS, ACUTE NECROTIZING; RECEPTORS, LIPOXIN; UP-REGULATION;

EID: 84896131269     PISSN: 21691401     EISSN: 2169141X     Source Type: Journal    
DOI: 10.3109/21691401.2013.794355     Document Type: Article

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