These authors contributed equally to this work.
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Salvianolic acid B suppresses maturation of human monocyte-derived dendritic cells by activating PPARγ
Article first published online: 21 NOV 2011
DOI: 10.1111/j.1476-5381.2011.01518.x
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society
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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
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These authors contributed equally to this work.
Publication History
- 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
Keywords:
- salvianolic acid B;
- dendritic cell;
- PPARγ;
- TLR4;
- atherosclerosis
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.