Conflict of interest: none to declare.
Original Research Article
Article first published online: 28 JAN 2013
Copyright © 2012 Wiley Periodicals, Inc.
Journal of Cellular Physiology
Volume 228, Issue 5, pages 975–982, May 2013
How to Cite
Yang, E.-J., Ku, S.-K., Lee, W., Lee, S., Lee, T., Song, K.-S. and Bae, J.-S. (2013), Barrier protective effects of rosmarinic acid on HMGB1-induced inflammatory responses in vitro and in vivo. J. Cell. Physiol., 228: 975–982. doi: 10.1002/jcp.24243
Eun-Ju Yang, Sae-Kwang Ku, and Wonhwa Lee contributed equally to this work.
- Issue published online: 28 JAN 2013
- Article first published online: 28 JAN 2013
- Accepted manuscript online: 5 OCT 2012 07:48AM EST
- Manuscript Accepted: 26 SEP 2012
- Manuscript Received: 29 MAY 2012
- National Research Foundation of Korea (NRF). Grant Number: 2012-0009400
- Korean Health Technology R&D Project
- Ministry of Health & Welfare, Republic of Korea. Grant Number: A111305
High mobility group box 1 (HMGB1) protein is a crucial cytokine that mediates response to infection, injury, and inflammation. Rosmarinic acid (RA) is an important component of the leaves of Perilla frutescens and has neuroprotective, anti-microbial, anti-oxidant, and anti-cancer effects but little is known of its effects on HMGB1-mediated inflammatory response. Here, we investigated this issue by monitoring the effects of RA on the lipopolysaccharide (LPS) or cecal ligation and puncture (CLP)-mediated release of HMGB1 and HMGB1-mediated modulation of inflammatory responses. RA potently inhibited the release of HMGB1 and down-regulated HMGB1-dependent inflammatory responses in human endothelial cells. RA also inhibited HMGB1-mediated hyperpermeability and leukocyte migration in mice. Furthermore, RA reduced CLP-induced HMGB1 release and sepsis-related mortality. Given these results, RA should be viewed as a candidate therapeutic agent for the treatment of various inflammatory diseases via inhibition of the HMGB1 signaling pathway. J. Cell. Physiol. © 2012 Wiley Periodicals, Inc.