中文摘要：

目的探讨免疫球蛋白IgG对H：O：诱导的内皮细胞的黏附分子和趋化因子的表达及作用机制。方法IgG和H，0，加入内皮细胞中孵育2h，应用RT—PCR以及实时定量RT—PCR检测黏附因子（ICAM—1、VCAM-1、E—se．1ectin）及趋化因子（MCP-1、CXCL—1、MIP-2）的mRNA及蛋白表达；进一步应用Westernblot检测IgG对H，0，诱导的p38、ERKI／2和JNKI／2的磷酸化情况。结果H2O2可显著诱导黏附分子（ICAM—1、VCAM．1和E—selectin）、趋化因子（MCP-1、CXCL—1、MIP-2）的表达，而IgG对H2O：诱导的这些因子的表达有抑制作用；且IgG可抑制H：0：诱导的p38、JNKI／2和ERK1／2的磷酸化。结论IgG对H2O，诱导的内皮细胞黏附分子及趋化因子表达的抑制作用可能通过抑制p38、JNK1／2、ERK1／2的信号通路实现，这可能是IgG调节内皮细胞炎症的机制之一。

英文摘要：

Purpose To explore the effect of immunoglobulin （IgG） on the expression of adhesion molecules and chemokines in HEOE-induced endothelial cells（ECs） and possible mechanism. Methods - Different concentrations IgG and H2O2 were added to ECs for 2 h. The levels of adhesion molecules （ICAM-1 ,VCAM-1 ,E-selectin） and chemokines（ MCP-1, CXCL-1, MIP-2） were determined by RT-PCR and quantitative RT-PCR. Furthermore the effect of IgG on the expression of p38, JNK1/2, ERK1/2 in H2O2 -induced ECs was determined by Western blot analysis. Results IgG dose-dependently inhibited the production of adhesion moleculus （ ICAM-1, VCAM-1, E-selectin ） and chemokines （ MCP-1, CXCL-1, MIP-2） in the activated ECs induced by H2O2. Conclusion The inhibitory effect of IgG on adhesion mol- ecules,chemokines expression induced by H2O2 in ECs might be mediated by p38 ,JNK1/2,ERK1/2 sig- naling pathways.