Article Publish Status: FREE
Abstract Title:

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

Abstract Source:

Mol Cells. 2013 Apr ;35(4):348-54. Epub 2013 Apr 4. PMID: 23563799

Abstract Author(s):

Eun Sun Seo, Bo Kang Oh, Jhang Ho Pak, Soon-Ho Yim, Sangilyandi Gurunathan, Young-Pil Kim, Kyung Jin Lee

Article Affiliation:

Eun Sun Seo


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.

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