Linked Life Data

20705587

Source:http://linkedlifedata.com/resource/pubmed/id/20705587

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2010-8-13
pubmed:abstractText
Accumulating data suggested that hypoxia inducible factor (HIF)-1alpha plays an important role in the evolution and propagation of the inflammatory process. To characterize the activation of HIF-1alpha in rats with chronic obstructive pulmonary disease (COPD) and examine the possible role of nuclear factor (NF)-kappaB in this process, rats were challenged by introtracheal instillation of lipopolysaccharide (LPS) and exposure to cigarette smoke. Pyrrolidine dithiocarbamate (PDTC) was administered via the oral route 1 h before LPS or cigarettes administration. Four weeks later, pulmonary function and histology were tested; bronchoalveolar lavage fluid (BALF) and arterial blood gases were assayed. Activation of pulmonary NF-kappaB was assessed by quantitative PCR, immunoblot analysis, and electrophoretic mobility shift assay, respectively. Results showed that LPS and smog induced the characteristics of COPD seen in human. PDTC alleviated the development of COPD and the levels of cytokines in BALF of PDTC+COPD group were significantly decreased compared with that of COPD group. The activation of pulmonary NF-kappaB was inhibited by PDTC and the accumulation of HIF-1alpha gene expression in the COPD group was attenuated by PDTC pretreatment. Furthermore, the mRNA levels of HIF-1alpha target genes heme oxygenase-1 (HO-1) and vascular endothelial growth factor (VEGF) were parallel to the attenuation of HIF-1alpha by PDTC. These findings indicated that the activation of HIF-1alpha pathway via NF-kappaB contributes to the development of COPD, and administration of NF-kappaB inhibitor may attenuate the development of COPD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1745-7270
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
483-8
pubmed:meshHeading
pubmed-meshheading:20705587-Administration, Oral, pubmed-meshheading:20705587-Animals, pubmed-meshheading:20705587-Antioxidants, pubmed-meshheading:20705587-Blood Gas Analysis, pubmed-meshheading:20705587-Bronchoalveolar Lavage Fluid, pubmed-meshheading:20705587-Cytokines, pubmed-meshheading:20705587-Heme Oxygenase-1, pubmed-meshheading:20705587-Hypoxia-Inducible Factor 1, alpha Subunit, pubmed-meshheading:20705587-Immunoblotting, pubmed-meshheading:20705587-Lipopolysaccharides, pubmed-meshheading:20705587-Lung, pubmed-meshheading:20705587-Male, pubmed-meshheading:20705587-NF-kappa B, pubmed-meshheading:20705587-Pulmonary Disease, Chronic Obstructive, pubmed-meshheading:20705587-Pyrrolidines, pubmed-meshheading:20705587-Rats, pubmed-meshheading:20705587-Rats, Sprague-Dawley, pubmed-meshheading:20705587-Respiratory Function Tests, pubmed-meshheading:20705587-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:20705587-Smoke, pubmed-meshheading:20705587-Thiocarbamates, pubmed-meshheading:20705587-Tobacco, pubmed-meshheading:20705587-Vascular Endothelial Growth Factor A
pubmed:year
2010
pubmed:articleTitle
Activation of hypoxia-inducible factor-1alpha via nuclear factor-kappa B in rats with chronic obstructive pulmonary disease.
pubmed:affiliation
Department of Anesthesiology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't