Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 431, Issue 3, Pages 506-511Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2012.12.143
Keywords
Berberine; Inflammation; Heme oxygenase-1; Nitric oxide synthase; High-mobility group box 1; Macrophage
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Funding
- Basic Science Research Program through the National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2012R1A1A2008714]
- Asan Institute for Life Sciences, Seoul, Korea [2012-505]
- National Research Foundation of Korea [2012R1A1A2008714] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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We investigated the molecular mechanism by which berberine reduces nitric oxide (NO) expression and high-mobility group box 1 (HMGB1) release in lipopolysaccharide (LPS)-induced macrophages. Berberine significantly inhibited the LPS-stimulated NO production and HMGB1 release in macrophages. In addition, berberine also induced heme oxygenase (HO)-1 in a dose-dependent manner, which was mediated through activation of p38 MAPK and NF-E2-related factor 2 (Nrf2) signaling cascade in macrophages. The inhibitory effect of berberine on LPS-stimulated NO and HMGB1 release was reversed by siRNA-Nrf2, SB203580 (p38 MAPK inhibitor) and zinc protoporphyrin (ZnPP; HO-1 inhibitor) within macrophages. Therefore, we conclude that berberine inhibits the proinflammatory response to LPS in macrophages by up-regulation of the HO-1 level, in which p38 MAPK and Nrf2 have an important role. These results suggest that berberine may be useful as a therapeutic agent for the treatment of inflammatory diseases. Crown Copyright (C) 2013 Published by Elsevier Inc. All rights reserved.
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