Protective effect of nerolidol on lipopolysaccharide-induced acute lung injury through the inhibition of NF-κB activation by the reduction of p38 MAPK and JNK phosphorylation

doi:doi.org/10.1016/j.jff.2020.103943

中山醫學大學機構典藏 CSMUIR > 醫學院 > 醫學系 > 期刊論文 > Item 310902500/22379

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題名:	Protective effect of nerolidol on lipopolysaccharide-induced acute lung injury through the inhibition of NF-κB activation by the reduction of p38 MAPK and JNK phosphorylation
作者:	Chen, Shih-Pin;Su, Chun-Hung;Rosa, Huang-Liu;Lee, Min-Wei;Chian, Chen-Yu;Chen, Wen-Ying;Chen, Chun-Jung;Wu, Sheng-Wen;Kuan, Yu-Hsiang
關鍵詞:	Nerolidol;LPSA;cute lung injury;NF-κB;p38 MAPK;JNK
日期:	2020-06
上傳時間:	2022-06-06T02:33:56Z (UTC)
出版者:	Elsevier Inc.
摘要:	Acute 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.
URI:	https://ir.csmu.edu.tw:8080/handle/310902500/22379
關聯:	Journal of Functional Foods, Volume 69, 103943
顯示於類別:	[醫學系] 期刊論文

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