[Study on expression of liver X receptor-alpha in rat lung tissue in acute lung injury].
OBJECTIVE
To observe changes in liver X receptor-alpha (LXR alpha) in acute lung injury (ALI) in rats induced by lipopolysaccharide (LPS) to explore mechanism of LXR alpha in pathogenesis of ALI.


METHODS
Forty-eight Wistar rats were randomly divided into two groups. ALI model was reproduced by intravenous injection of LPS (5 mg/kg), and control group was injected with normal saline (2.5 ml/kg). At 1, 2, 4, 8 hours after ALI, artery blood gas analysis, lung tissue wet/dry weight (W/D) ratio, myeloperoxidase (MPO) activity, lung histopathologic changes were observed. The expressions of LXR alpha and tumor necrosis factor-alpha (TNF-alpha) mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR). TNF-alpha content was measured with enzyme linked immunosorbent assay (ELISA). LXR alpha protein in lung tissues was assessed by immunohistochemistry.


RESULTS
Compared with the control group, in ALI rats at different time points, partial pressure of oxygen in arterial blood (PaO(2)) decreased significantly, lung W/D weight ratio and MPO activity increased significantly (all P<0.05), histopathology of lung revealed signs of injury. After injury, expression of LXR alpha mRNA in lung tissue decreased markedly, and expression of TNF-alpha mRNA in lung tissue increased markedly (all P<0.05). TNF-alpha increased markedly in lung homogenate and blood serum at the same period, and TNF-alpha reached peak value at 4 hours. Immunohistochemical staining of LXR alpha showed that lung tissues of normal rats express LXR alpha significantly, however, after injury, expression of LXR alpha in lung tissue decreased markedly (all P<0.05).


CONCLUSIONS
Lung tissues of normal rats express LXR alpha. The decreased LXR alpha mRNA and protein expressions in the lung tissue of rats with ALI caused by LPS may be associated with the occurrence of ALI.
Institute of Respiratory Medicine of PLA, Xinqiao Hospital, the Third Military Medical University, Chongqing 400037, China.
Jing
J
Xu
Jian-chun
JC
Wang
Bo
B
Xiao
Guan-song
GS
Wang
D055371:Acute Lung Injury / Q000139:chemically induced / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D008070:Lipopolysaccharides / Q000633:toxicity; D000071518:Liver X Receptors; D008168:Lung / Q000378:metabolism* / Q000473:pathology; D008297:Male; D057093:Orphan Nuclear Receptors / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics
D008070:Lipopolysaccharides; D000071518:Liver X Receptors; C000605215:Nr1h3 protein, rat; D057093:Orphan Nuclear Receptors; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha