AIM: Vaticanol(B,C and G),α-viniferin and hopeaphenol are resveratrol oligomers,which are documented to possess antitumor,antioxidative activities,and chemoprotective effects attributed to their anti-inflammatory activities.The present study was aimed at evaluating their effects on the release of histamine,tumor necrosis factor-α (TNF-α) and leukotrienes (LTs) from bone marrow-derived mast cells (BMMC) in vitro.Meanwhile,activation of extracellular signal-regulated kinases (ERK) was also investigated.METHOD: BMMC were prepared by isolating bone marrow cells from intact femurs(Balb/c mice) and culturing them for 4-5 weeks in RPMI-1640 medium,supplemented with 10% FCSand IL-3 (10 ng/ml).BMMC were sensitized with anti-DNP IgE and stimulated with DNP-BSA (30 ng/ml) to trigger release reaction.In the nonimmunological stimulation experiments,BMMC were directly stimulated with calcium ionophore A23187 (3.0 μmol/L).RESULT:All compounds examined showed inhibitory effects on mediator release from BMMC to a certain extent.In the release reaction mediated by IgE,both TNF-α and LTs were significantly reduced by above compounds in a concentration-dependent manner.Vaticanol B and C inhibited IgE-mediated histamine release at a concentration of 100 μmol/L.A23187-mediated histamine release was potently inhibited by vaticanol (B,C and G) and hopeaphenol,but not by α-viniferin.Most of the tested compounds substantially reduced TNF-α and LTs production mediated by IgE or A23187,but vaticanol C and G did not exhibit effective inhibition of A23187-mediated LTs release.IgE-mediated activation of ERK was strongly inhibited by α-viniferin and vativanol C.Incubated with above compounds for 48 hours,cell viability of BMMC was not influenced.CONCLUSION:Vaticanol (B,C and G),α-viniferin,and hopeaphenol are potent inhibitors of inflammatory mediator release from mast cells and without significant influence on the cell viability of BMMC.%目的:α-viniferin, vaticanol(B, C and G) 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-1640,IL-3 10 ng/ml),抗-DNP IgE 致敏,以DNP-BSA(30 ng/ml)刺激释放反应.在非免疫刺激释放实验中,A23187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vaticanol B和vaticanol C 具有抑制作用(100 μmol/L).在A23187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vaticanol C和vaticanol G对LTs的释放无明显影响.α-viniferin和vaticanol C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
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