title: Paeoniflorin inhibits function and down-regulates HLA-DR and CD80 expression of human peripheral blood monocytes stimulated by rhIL-1β.
abstract: 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-1β (rhIL-1β)-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-1β to imitate inflammatory circumstance in vitro. After exposure of rhIL-1β (0.01, 0.1, 1, 10 μg·l(-1)) for 24h or rhIL-1β (1 μg·l(-1)) for different time periods (3, 6, 12, 24h), we observed that the phagocytic function and the production of TNF-α and PGE(2) with monocytes were promoted significantly by rhIL-1β. MTT assay demonstrated that paeoniflorin (concentrations ranged from 10(-4)mol·l(-1) to 10(-9)mol·l(-1)) showed low cytotoxicity with rhIL-1β-stimulated monocytes. Paeoniflorin (10(-9), 10(-8), 10(-7), 10(-6), 10(-5)mol·l(-1)) significantly suppressed phagocytic function of rhIL-1β-induced monocytes (P<0.05), and decreased the levels of TNF-α 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-1β 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(-6), 10(-5)mol·l(-1)) significantly inhibited the mean fluorescence rates of HLA-DR and CD80 with rhIL-1β-stimulated monocytes (P<0.05). These results indicated that paeoniflorin might inhibit activation of human peripheral blood monocytes stimulated by rhIL-1β, 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.
authors: Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immunopharmacology of Ministry of Education of PR China, Meishan Road, Hefei 230032, Anhui Province, PR China. wangdi.ahmu@gmail.com
authors: Di
authors: D
authors: Wang
authors: Fang
authors: F
authors: Yuan
authors: Liwen
authors: L
authors: Wang
authors: Wei
authors: W
authors: Wei
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D018122:B7-1 Antigen / Q000378:metabolism*; D001565:Benzoates / Q000494:pharmacology*; D001952:Bridged-Ring Compounds / Q000494:pharmacology*; D015232:Dinoprostone / Q000378:metabolism; D015536:Down-Regulation; D005960:Glucosides / Q000494:pharmacology*; D006684:HLA-DR Antigens / Q000378:metabolism*; D006801:Humans; D053583:Interleukin-1beta / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000276:immunology; D039821:Monoterpenes; D010587:Phagocytosis / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D006027:Glycosides
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D018122:B7-1 Antigen; D001565:Benzoates; D001952:Bridged-Ring Compounds; D015232:Dinoprostone; D005960:Glucosides; D006684:HLA-DR Antigens; D053583:Interleukin-1beta; D039821:Monoterpenes; D014409:Tumor Necrosis Factor-alpha; C015423:peoniflorin; D006027:Glycosides