SHIH-PIN CHENCHUN-HUNG SUSHENG-WEN WUYU-HSIANG KUAN2026-10-162026-10-162020-06-01Pure ID: 15008801Pure UUID: 10c5ebe6-c180-4f33-b16d-3253fff1f26a10.1016/j.jff.2020.103943https://www.scopus.com/pages/publications/85082861655https://scholars.csmu.edu.tw/handle/123456789/24213Acute lung injury (ALI) is a severe syndrome, and there are no effective therapeutic appropriate medicines. Nerolidol, which exists in the essential oils of aromatic plants and flowers, exhibits antioxidative and anti-inflammatory activities. The present study evaluated the potential protective effect of nerolidol in ALI and the related mechanism in lipopolysaccharide (LPS)-treated mice. Here, nerolidol inhibited the LPS-induced neutrophil and other leukocyte infiltration of the alveolar space. LPS increased cytokines, chemokines, and adhesion molecules, and proinflammatory protein production was inhibited by nerolidol. LPS-induced phosphorylation of NF-κB p65, p38 MAPK, JNK, ERK were inhibited by nerolidol. The inhibitory concentration of nerolidol for the phosphorylation of NF-κB p65 and its upstream factors, p38 MAPK and JNK, was similar to the inflammatory responses of ALI. In conclusion, nerolidol is a potential protective agent in ALI via the inhibition of NF-κB activation and its upstream factors phosphorylation of p38 MAPK and JNK.enProtective effect of nerolidol on lipopolysaccharide-induced acute lung injury through the inhibition of NF-κB activation by the reduction of p38 MAPK and JNK phosphorylationjournal article