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目的 :α viniferin ,vaticanol(B ,CandG)和hopeaphenol是白黎芦醇的低聚体 ,具有抗肿瘤和抗氧化等活性 ,而这些化学保护作用是与其抗炎作用有联系。本文研究旨在了解这些化合物对小鼠骨髓分化肥大细胞 (BMMC)组织胺、肿瘤坏死因子和白三烯介质释放的影响 ,并观察对细胞外信号调节激酶 (ERK)的激活作用。方法 :分离小鼠骨髓细胞 ,培养 4～ 5周 (RPMI 16 4 0 ,IL 310ng/ml) ,抗 DNPIgE致敏 ,以DNP BSA( 30ng/ml)刺激释放反应。在非免疫刺激释放实验中 ,A2 3187作为刺激剂。结果 :所试化合物均表现出不同程度的抑制BMMC释放反应的作用。这些化合物对IgE刺激的TNF α和LTs释放表现出显著的抑制作用 ,而对IgE刺激的组织胺释放反应 ,只有vaticanolB和vaticanolC具有抑制作用 ( 10 0μmol/L)。在A2 3187介导的非免疫刺激释放反应中 ,vaticanol(B ,C和G)和hopeaphenol对组织胺释放表现出明显的对抗作用 ,大多数所试化合物有效地抑制了TNF α和LTs的释放 ,唯vaticanolC和vaticanolG对LTs的释放无明显影响。α viniferin和vaticanolC有效地抑制了IgE刺激的ERK酶的激活。结论 :α viniferin ,vaticanol(B ,C和G)和hopeaphenol能有效地抑制肥大细胞的炎性介质的释放反应 ,而对BMMC的细胞活力无明显影响
Objectives: α viniferin, vaticanol (B, CandG) and hopeaphenol are oligomers of resveratrol and have anti-tumor and anti-oxidant activities, and these chemical protective effects are related to their anti-inflammatory effects. The purpose of this study was to understand the effects of these compounds on the release of histamine, tumor necrosis factor, and leukotrienes from mouse bone marrow-derived mast cells (BMMC), and to observe the activation of extracellular signal-regulated kinase (ERK). METHODS: Mouse bone marrow cells were isolated, cultured for 4 to 5 weeks (RPMI 16 4 0, IL 310 ng/ml), sensitized to DNPIgE, and stimulated by DNP BSA (30 ng/ml). In non-immunostimulatory release experiments, A2 3187 was used as a stimulator. Results: All tested compounds showed different degrees of inhibition of BMMC release. These compounds exhibited significant inhibitory effects on IgE-stimulated TNFα and LTs release, whereas only vaticanolB and vaticanolC had an inhibitory effect on IgE-stimulated histamine release (100 μmol/L). In the A2 3187-mediated non-immunostimulatory release response, vaticanol (B, C, and G) and hopeaphenol exhibited significant antagonistic effects on histamine release, and most of the tested compounds effectively inhibited the release of TNFα and LTs. Only vaticanolC and vaticanolG had no significant effect on the release of LTs. Alpha viniferin and vaticanolC effectively inhibited the activation of IgE-stimulated ERK enzymes. Conclusion : α viniferin, vaticanol (B, C and G) and hopeaphenol can effectively inhibit the release response of inflammatory mediators of mast cells without significant effect on the cell viability of BMMC.