Decreased Expression of
Peroxisome Proliferator-Activated Receptor γ in
Endotoxin-Induced Acute Lung Injury
D. LIU1, B. XIONG ZENG2, Y.
SHANG2
1Department of Anesthesiology and Critical Care
Medicine, Lanzhou General Hospital of P.L.A., Lanzhou, 2Department
of Anesthesiology, Union Hospital, Tongji Medical College,
Huazhong University of Science and Technology, Wuhan, China
Received June 23, 2005
Accepted August 5, 2005
On-line available August 8, 2005
Summary
Peroxisome proliferator-activated receptor-γ (PPAR- γ), a member
of the nuclear hormone receptor superfamily of ligand-activated
transcription factors, possesses anti-inflammatory properties.
The purpose of the present study was to investigate the profile
of PPAR- γ expression in the lung and to explore its functional
significance in lipopolysaccharide (LPS)-induced acute lung
injury. Thirty male Wistar rats were randomly assigned to one of
the following five groups: saline control group and different
LPS groups (2 h, 4 h, 6 h and 8 h after LPS 6 mg/kg i.v.). At
predefined time points, blood samples were collected to measure
plasma level of tumor necrosis factor (TNF)-α and lungs were
removed to assay histopathological changes, wet-to-dry weight
(W/D) ratio, myeloperoxidase (MPO) activity and TNF-α level.
Expression of PPAR- γ and activation of nuclear factor (NF)- κB
p65 in lung tissues were also examined in each group. LPS
injection resulted in marked lung damage and elevated levels of
W/D ratio and MPO activity in the lung. Increased levels of
TNF-α were also observed in the plasma and lung. These
inflammatory events were associated with reduced expression of
PPAR-γ protein and with activation of NF-κB in the lung. Our
data suggest that decreased expression of PPAR-γ protein in
lungs may contribute to the ongoing pulmonary inflammation and
tissue injury in endotoxemia.
Key words
Peroxisome proliferator-activated receptor- • Endotoxin • Acute
lung injury • Nuclear factor-B
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