PPAR-α improves the recovery of lung function following acute respiratory distress syndrome by suppressing the level of TGF-β1.

Although peroxisome proliferator-activated receptor (PPAR)-α 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‑α prevents ALI and examine the role of PPAR‑α 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‑α was effective in suppressing transforming growth factor (TGF)‑β1 in HLF cells and RAW 264.7 cells. In an ALI mouse model, PPAR‑α treatment prior to stimulation with lipopolysaccharide (LPS) resulted in a decrease in the expression of TGF‑β1 in bronchoalveolar lavage fluid (BALF), peripheral blood and splenocytes. The injection of a virus expressing short hairpin PPAR‑α 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‑α was essential for the recovery of lung function following ALI. Of note, the serum expression of PPAR‑α was inversely correlated with TGF‑β1 and negatively correlated with disease severity in patients with ARDS. These data suggested that PPAR‑α was essential for the recovery of lung function following ALI by the suppression of TGF‑β1, which reveals a previously unappreciated mechanism controlling post‑ALI lung recovery.