Abstract
Acute respiratory distress syndrome is a well-known inflammatory disease associated with high rates of morbidity and mortality due to a lack of effective treatment methods. Carnosic acid (CA) is a phenolic diterpene compound that serves a central role in cytoprotective responses to inflammation. In the present study, the protective mechanism of CA on acute lung injury (ALI) induced by lipopolysaccharide (LPS) was investigated. Mice were randomly assigned to the following five groups: Control group, LPS group, and LPS plus CA groups (at 10, 20 and 40 mg/kg doses). Following pre-treatment with vehicle or CA, ALI was induced by the administration of LPS. At 6 h after LPS treatment, mice were sacrificed and lung tissues were harvested for histologic analysis and the determination of wet-to-dry ratio, myeloperoxidase activity and toll-like receptor 4 (TLR4) and NF-κB expression. Additionally, the levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) were determined in bronchoalveolar lavage fluid (BALF) and lung tissues, as well as the rate of apoptosis of the isolated neutrophils from BALF. The alleviation of LPS-induced ALI by CA was confirmed by histologic results and a reduction in the wet-to-dry ratio of lung tissues. Additionally, CA was revealed to significantly suppress the inhibitory effect of LPS on neutrophil apoptosis and the promoting effects of LPS on IL-1β, IL-6, TNF-α, TLR4 and NF-κB expression, and NF-κB phosphorylation. The current results indicated that CA protects against LPS-induced ALI via a mechanism that inhibits inflammation.