These authors contributed equally to this work.
Wogonin attenuates endotoxin-induced prostaglandin E2 and nitric oxide production via Src-ERK1/2-NFκB pathway in BV-2 microglial cells
Article first published online: 30 JAN 2013
Copyright © 2013 Wiley Periodicals, Inc., a Wiley company
Volume 29, Issue 10, pages 1162–1170, October 2014
How to Cite
Yeh, C.-H., Yang, M.-L., Lee, C.-Y., Yang, C.-P., Li, Y.-C., Chen, C.-J. and Kuan, Y.-H. (2014), Wogonin attenuates endotoxin-induced prostaglandin E2 and nitric oxide production via Src-ERK1/2-NFκB pathway in BV-2 microglial cells. Environ. Toxicol., 29: 1162–1170. doi: 10.1002/tox.21847
- Issue published online: 5 SEP 2014
- Article first published online: 30 JAN 2013
- Manuscript Accepted: 27 DEC 2012
- Manuscript Revised: 25 DEC 2012
- Manuscript Received: 4 OCT 2012
- National Science Council of the Republic of China, Taiwan. Grant Number: NSC99-2320-B-040-012-MY3
- Show Chwan Health Care System of the Republic of China, Taiwan. Grant Number: RD100029 and RD101019
Microglia are the major component of intrinsic brain immune system in neuroinflammation. Although wogonin expresses anti-inflammatory function in microglia, little is known about the molecular mechanisms of the protective effect of wogonin against microglia activation. The aim of this study was to evaluate how wogonin exerts its anti-inflammatory function in BV2 microglial cells after LPS/INFγ administration. Wogonin not only inhibited LPS/ INFγ-induced PGE2 and NO production without affecting cell viability but also exhibited parallel inhibition on LPS/INFγ-induced expression of iNOS and COX-2 in the same concentration range. While LPS/INFγ-induced expression of P-p65 and P-IκB was inhibited by wogonin—only weak inhibition on P-p38 and P-JNK were observed, whereas it significantly attenuated the P-ERK1/2 and its upstream activators P-MEK1/2 and P-Src in a parallel concentration-dependent manner. These results indicated that the blockade of PGE2 and NO production by wogonin in LPS/INFγ-stimulated BV2 cells is attributed mainly to interference in the Src-MEK1/2-ERK1/2-NFκB-signaling pathway. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1162–1170, 2014.