Abietic acid attenuates LPS-induced acute lung injury by restoring Th17/Treg balance

Abstract

Purpose: To investigate the mechanism of action and effects of abietic acid (AA) in a mouse acute lung injury (ALI) model. Methods: A mouse ALI model was established by lipopolysaccharide (LPS) induction. Lung tissues were examined for histological alterations and scored based on the degree of injury. Myeloperoxidase (MPO), IL-6, IL-1β, and TNF-α levels were measured by enzyme-linked immunosorbent assay (ELISA) while the numbers of Th17 and Treg cells were assessed by immunofluorescence. Protein expression levels of p-STAT3, p-STAT5, RORrt, and FOXP3 were analyzed by immunoblot assay. Expression of peroxisome proliferator-activated receptor γ (PPARγ) was assessed by immunoblot. Results: AA ameliorated LPS-induced lung injury in mice. Furthermore, AA ameliorated LPS-induced pneumonia in mice (p < 0.05) and restored Th17/Treg balance and Th17/Treg transcription factor expression that was altered by LPS induction. AA also activated PPARγ expression to restore Th17/Treg balance (p < 0.05). Conclusion: The results indicate that AA attenuates LPS-induced ALI in mice by restoring Th17/Treg balance. Thus, AA is a potential drug for the management of ALI; however, AA must first be evaluated in clinical studies.