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Bioflavonoid Quercetin Inhibits Interleukin-1-Induced Transcriptional Expression of Monocyte Chemoattractant Protein-1 in Glomerular Cells via Suppression of Nuclear Factor-B

YOSHIHISA ISHIKAWA^*, HITOSHI SUGIYAMA, ELENI STYLIANOU and MASANORI KITAMURA^*

^* Glomerular Bioengineering Unit, Department of Medicine, University College London Medical School, London
Division of Renal and Inflammatory Disease, School of Medical and Surgical Sciences, University Hospital, Nottingham, United Kingdom.

Correspondence to Dr. Masanori Kitamura, Department of Medicine, University College London Medical School, The Rayne Institute, 5 University Street, London WC1E 6JJ, United Kingdom. Phone: +44 171 209 6191; Fax: +44 171 209 6211; E-mail: m.kitamura{at}medicine.ucl.ac.uk

Abstract. Flavonoids are semiessential food components that possess anti-inflammatory properties. This report describes a novel potential of bioflavonoid quercetin as an inhibitor of monocyte chemoattractant protein-1 (MCP-1) in glomerular cells. Cultured mesangial cells as well as isolated glomeruli expressed MCP-1 mRNA in response to interleukin-1ß (IL-1ß). Quercetin dramatically inhibited the cytokine-triggered MCP-1 expression. To explore the mechanisms involved, effects of quercetin on the putative transcriptional activators of MCP-1, nuclear factor-B (NF-B) and activator protein-1 (AP-1), were examined. Exposure of the cells to IL-1ß caused activation of NF-B without significant upregulation of AP-1 activity. NF-B inhibitor MG132 diminished the IL-1-induced expression of MCP-1 in mesangial cells and isolated glomeruli, whereas c-Jun/Ap-1 inhibitor curcumin did not affect this process. Consistently, NF-B-inactive mesangial cells expressing a super-repressor mutant of IB showed blunted expression of MCP-1 by IL-1ß. In contrast, AP-1-inactive mesangial cells expressing a dominant-negative mutant of c-Jun exhibited the same level of MCP-1 mRNA as that in control cells. These results suggest that: (1) quercetin has the ability to attenuate activation of NF-B; and (2) it inhibits IL-1-triggered MCP-1 expression via suppression of NF-B, but not AP-1, in glomerular cells.

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