Structured triglyceride attenuates lung injury and inflammation in lipopolysaccharide‑induced acute lung injury by enhancing GPR120 expression.

Abstract

Acute lung injury(ALI) is a serious clinical problem. The present study was performed to investigate the effect of structured triglyceride(STG) on the development of lipopolysaccharide(LPS)‑induced ALI and its underlying mechanism of action. To establish an LPS‑induced ALI mouse model, mice were intranasally administered 50µl LPS. The pathological changes in the lung were observed via haematoxylin‑eosin staining. The lung injury score, lung wet/dry weight(W/D) ratio, and myeloperoxidase(MPO) activity were used to evaluate the degree of lung injury. The expression levels of interleukin(IL)‑1β, IL‑6 and tumour necrosis factor‑α in lung tissues were measured through reverse transcription‑quantitative polymerase chain reaction. The enzyme‑linked immunosorbent assay was used to measure the levels of pro‑inflammatory cytokines in bronchoalveolar lavage fluid. Furthermore, western blotting was performed to detect the activity of the transforming growth factor‑α‑activated kinase1(TAK1)/NF‑κB pathway. LPS‑induced ALI mice were treated with AH7614 [a G‑protein coupled receptor 120 (GPR120) inhibitor] to confirm the effect of STG on GPR120. STG treatment decreased the lung pathological changes, lung injury score, lung W/D ratio, and proinflammatory cytokine expression levels and inhibited TAK1/NF‑κB pathway activity in the LPS‑induced ALI mouse model. Additionally, AH7614 reversed the inhibitory effects of STG on lung injury, inflammation, and TAK1/NF‑κB pathway activity in ALI. Moreover, AH7614 weakened the inhibitory effects of STG on inflammation and TAK1/NF‑κB pathway activity in LPS‑induced RAW264.7 cells. Collectively, STG may suppress the TAK1/NF‑κB pathway activity by enhancing GPR120 expression to alleviate the lung injury and inflammation in ALI. These results suggest the therapeutic potential of STG in the treatment of ALI.