These authors contributed equally to this work.
Salvianolic acid B suppresses maturation of human monocyte-derived dendritic cells by activating PPARγ
Article first published online: 21 NOV 2011
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society
British Journal of Pharmacology
Volume 164, Issue 8, pages 2042–2053, December 2011
How to Cite
Sun, A., Liu, H., Wang, S., Shi, D., Xu, L., Cheng, Y., Wang, K., Chen, K., Zou, Y. and Ge, J. (2011), Salvianolic acid B suppresses maturation of human monocyte-derived dendritic cells by activating PPARγ. British Journal of Pharmacology, 164: 2042–2053. doi: 10.1111/j.1476-5381.2011.01518.x
- Issue published online: 21 NOV 2011
- Article first published online: 21 NOV 2011
- Accepted manuscript online: 7 JUN 2011 08:47AM EST
- Received; 13 June 2010; Revised; 20 April 2011; Accepted; 19 May 2011
- salvianolic acid B;
- dendritic cell;
BACKGROUND AND PURPOSE Salvianolic acid B (Sal B), a water-soluble antioxidant derived from a Chinese medicinal herb, is known to be effective in the prevention of atherosclerosis. Here, we tested the hypothesis that the anti-atherosclerotic effect of Sal B might be mediated by suppressing maturation of human monocyte-derived dendritic cells (h-monDC).
EXPERIMENTAL APPROACH h-monDC were derived by incubating purified human monocytes with GM-CSF and IL-4. h-monDC were pre-incubated with or without Sal B and stimulated by oxidized low-density lipoprotein (ox-LDL) in the presence or absence of PPARγ siRNA. Expression of h-monDC membrane molecules (CD40, CD86, CD1a, HLA-DR) were analysed by FACS, cytokines were measured by elisa and the TLR4-associated signalling pathway was determined by Western blotting.
KEY RESULTS Ox-LDL promoted h-monDC maturation, stimulated CD40, CD86, CD1a, HLA-DR expression and IL-12, IL-10, TNF-α production; and up-regulated TLR4 signalling. These effects were inhibited by Sal B. Sal B also triggered PPARγ activation and promoted PPARγ nuclear translocation, attenuated ox-LDL-induced up-regulation of TLR4 and myeloid differentiation primary-response protein 88 and inhibited the downstream p38-MAPK signalling cascade. Knocking down PPARγ with the corresponding siRNA blocked these effects of Sal B.
CONCLUSIONS AND IMPLICATIONS Our data suggested that Sal B effectively suppressed maturation of h-monDC induced by ox-LDL through PPARγ activation.