Acteoside improves survival in cecal ligation and puncture-induced septic mice via blocking of high mobility group box 1 release

Acteoside, an active phenylethanoid glycoside, has been used traditionally as an anti-inflammatory agent. The molecular mechanism by which acteoside reduces inflammation was investigated in lipopolysaccharide (LPS)-induced Raw264.7 cells and in a mouse model of cecal ligation and puncture (CLP)-indu...

Full description

Saved in:
Bibliographic Details
Published inMolecules and cells Vol. 35; no. 4; pp. 348 - 354
Main Authors Seo, Eun Sun, Oh, Bo Kang, Pak, Jhang Ho, Yim, Soon-Ho, Gurunathan, Sangilyandi, Kim, Young-Pil, Lee, Kyung Jin
Format Journal Article
LanguageEnglish
Published Springer Korean Society for Molecular and Cellular Biology 01.04.2013
Korea Society for Molecular and Cellular Biology
한국분자세포생물학회
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Acteoside, an active phenylethanoid glycoside, has been used traditionally as an anti-inflammatory agent. The molecular mechanism by which acteoside reduces inflammation was investigated in lipopolysaccharide (LPS)-induced Raw264.7 cells and in a mouse model of cecal ligation and puncture (CLP)-induced sepsis. In vitro , acteoside inhibits high mobility group box 1 (HMGB1) release and iNOS/NO production and induces heme oxygenase-1 (HO-1) expression in a concentration-dependent manner, while HO-1 siRNA antagonizes the inhibition of HMGB1 and NO. The effect of acteoside is inhibited by the p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 and Nfr2 siRNA, indicating that acteoside induces HO-1 via p38 MAPK and NF-E2-related factor 2 (Nrf2). In vivo , acteoside increases survival and decreases serum and lung HMGB1 levels in CLP-induced sepsis. Overall, these results that acteoside reduces HMGB1 release and may be beneficial for the treatment of sepsis.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 14
These authors contributed equally to this work.
G704-000079.2013.35.4.012
ISSN:1016-8478
0219-1032
DOI:10.1007/s10059-013-0021-1