Paeoniflorin inhibits function and down-regulates HLA-DR and CD80 expression of human peripheral blood monocytes stimulated by RhIL-1β

Paeoniflorin has been demonstrated to exert anti-inflammatory and immunomodulatory effects in the animal study. The purpose of the present study was to investigate the effect of paeoniflorin on the recombinant human interleukin-1 beta (rhIL-1 beta)-stimulated monocytes from the peripheral blood of healthy adults in vitro. Monocytes, collected from the peripheral blood of healthy adults by the Ficoll density gradient centrifugation, were co-cultured with rhIL-1 beta to imitate inflammatory circumstance in vitro. After exposure of rhIL-1 beta (0.01, 0.1, 1, 10 mu g.l(-1)) for 24 h or rhIL-1 beta (1 mu g.l(-1)) for different time periods (3, 6, 12, 24 h), we observed that the phagocytic function and the production of TNF-alpha and PGE(2) with monocytes were promoted significantly by rhIL-1 beta. MTT assay demonstrated that paeoniflorin (concentrations ranged from 10(-4) mol.l(-1) to 10(-9) mol.l(-1)) showed low cytotoxicity with rhIL-1 beta-stimulated monocytes. Paeoniflorin (10(-9), 10(-8), 10(-7), 10(-6), 10(-5) mol.l(-1)) significantly suppressed phagocytic function of rhIL-1 beta-induced monocytes (P<0.05), and decreased the levels of TNF-alpha and PGE(2) production in a concentration-dependent manner (r=-0.820 and r=-0.836, respectively). The flow cytometry analysis showed that the stimulation of rhIL-1 beta significantly increased the mean fluorescence rates of HLA-DR in a time-dependent manner (r=0.977). Administration of paeoniflorin (10(-9), 10(-8), 10(-7), 10(-8), 10(-5) mol.l(-1)) significantly inhibited the mean fluorescence rates of HLA-DR and CD80 with rhIL-1 beta-stimulated monocytes (P<0.05). These results indicated that paeoniflorin might inhibit activation of human peripheral blood monocytes stimulated by rhIL-1 beta, suppress function of monocytes, and down-regulate expression of HLA-DR and CD80, suggesting that paeoniflorin might alleviate the chronic inflammation by inhibiting human monocytes. (C) 2012 Elsevier B.V. All rights reserved.