Koo NaYeon, Cho DongIm, Kim YoungRan, Choi Hyun Jin, Kim Kyeong-Man
Department of Pharmacology, College of Pharmacy, Chonnam National University, Kwang-Ju, Korea.
Planta Med. 2006 Jun;72(7):659-61. doi: 10.1055/s-2006-931568. Epub 2006 Apr 24.
The molecular mechanism of how resveratrol inhibits mast cell degranulation was studied by examining its effects on the signaling components of the high affinity IgE receptor (FcepsilonRI) pathway. Resveratrol inhibited mast cell degranulation in a dose-dependent manner and reduced the FcepsilonRI-mediated tyrosine phosphorylation of ERK and PLCgamma1 but not of Syk and PLCgamma2. U-73 122 and PD98059, which are PLC and MEK inhibitors, also had inhibitory effects on mast cell degranulation. These results suggest that FcepsilonRI-mediated tyrosine phosphorylation of PLCgamma1 and ERK could be potential cellular targets of resveratrol for the inhibition of mast cell degranulation.
通过研究白藜芦醇对高亲和力IgE受体(FcepsilonRI)信号通路中信号成分的影响,探讨了其抑制肥大细胞脱颗粒的分子机制。白藜芦醇以剂量依赖性方式抑制肥大细胞脱颗粒,并降低FcepsilonRI介导的ERK和PLCgamma1的酪氨酸磷酸化,但不影响Syk和PLCgamma2的酪氨酸磷酸化。PLC和MEK抑制剂U-73 122和PD98059也对肥大细胞脱颗粒有抑制作用。这些结果表明,FcepsilonRI介导的PLCgamma1和ERK的酪氨酸磷酸化可能是白藜芦醇抑制肥大细胞脱颗粒的潜在细胞靶点。