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Paeoniflorin inhibits function and down-regulates HLA-DR and CD80 expression of human peripheral blood monocytes
Di Wang1, Fang Yuan, Liwen Wang
1Institute 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
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.
Insights
Paeoniflorin effectively suppresses the inflammatory response in human monocytes stimulated by recombinant human interleukin-1β (rhIL-1β). This natural compound inhibits monocyte function and reduces key inflammatory markers, suggesting potential for chronic inflammation treatment.
Area of Science:
- Immunology
- Pharmacology
- Cell Biology
Background:
- Paeoniflorin exhibits known anti-inflammatory and immunomodulatory effects in preclinical animal studies.
- Monocytes play a crucial role in inflammatory processes, and their activation by cytokines like interleukin-1β is a key feature of inflammation.
Purpose of the Study:
- To investigate the in vitro effects of paeoniflorin on human peripheral blood monocytes stimulated by recombinant human interleukin-1β (rhIL-1β).
Main Methods:
- Human monocytes were isolated and stimulated with rhIL-1β to mimic an inflammatory environment.
- Cellular functions including phagocytosis and production of TNF-α and PGE(2) were assessed.
- Cytotoxicity, cell surface marker expression (HLA-DR, CD80) via flow cytometry, and cell viability (MTT assay) were evaluated.
Main Results:
- rhIL-1β significantly enhanced monocyte phagocytic function and production of TNF-α and PGE(2).
- Paeoniflorin demonstrated low cytotoxicity and dose-dependently suppressed rhIL-1β-induced monocyte phagocytosis, TNF-α, and PGE(2) production.
- Paeoniflorin significantly inhibited the rhIL-1β-induced increase in HLA-DR and CD80 expression on monocytes.
Conclusions:
- Paeoniflorin inhibits the activation and function of human peripheral blood monocytes stimulated by rhIL-1β.
- The compound down-regulates key activation markers (HLA-DR, CD80) and inflammatory mediators (TNF-α, PGE(2)).
- These findings suggest paeoniflorin has therapeutic potential in alleviating chronic inflammatory conditions by modulating monocyte activity.
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