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Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Mol+Med+Rep 2017 ; 16 (1): 49-56 Nephropedia Template TP
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PPAR-? improves the recovery of lung function following acute respiratory distress syndrome by suppressing the level of TGF-?1 #MMPMID28498479
Liu Y; Xie L; Yang M; Tan X; Zeng Y; Zheng G; Chen Y; Chen P
Mol Med Rep 2017[Jul]; 16 (1): 49-56 PMID28498479show ga
Although peroxisome proliferator-activated receptor (PPAR)-? has been reported to be involved in preventing acute lung injury (ALI), the molecular regulation of post-ALI lung recovery remains to be fully elucidated. The aim of the present study was to characterize the mechanism by which PPAR-? prevents ALI and examine the role of PPAR-? in the recovery of lung function following acute respiratory distress syndrome (ARDS). Reverse transcription-quantitative-polymerase chain reaction and western blot analyses suggested that PPAR-? was effective in suppressing transforming growth factor (TGF)-?1 in HLF cells and RAW 264.7 cells. In an ALI mouse model, PPAR-? treatment prior to stimulation with lipopolysaccharide (LPS) resulted in a decrease in the expression of TGF-?1 in bronchoalveolar lavage fluid (BALF), peripheral blood and splenocytes. The injection of a virus expressing short hairpin PPAR-? into mice following LPS treatment resulted in a dose-dependent increase in lung resistance index and decrease in dynamic compliance, and a significant increase in BALF protein, which indicated PPAR-? was essential for the recovery of lung function following ALI. Of note, the serum expression of PPAR-? was inversely correlated with TGF-?1 and negatively correlated with disease severity in patients with ARDS. These data suggested that PPAR-? was essential for the recovery of lung function following ALI by the suppression of TGF-?1, which reveals a previously unappreciated mechanism controlling post-ALI lung recovery.