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目的探讨免疫球蛋白IgG对H2O2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H2O2加入内皮细胞中孵育2 h,应用RT-PCR以及实时定量RT-PCR检测黏附因子(ICAM-1、VCAM-1、E-se-lectin)及趋化因子(MCP-1、CXCL-1、MIP-2)的mRNA及蛋白表达;进一步应用Western blot检测IgG对H2O2诱导的p38、ERK1/2和JNK1/2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H2O2诱导的这些因子的表达有抑制作用;且IgG可抑制H2O2诱导的p38、JNK1/2和ERK1/2的磷酸化。结论 IgG对H2O2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。
Objective To investigate the effect of immunoglobulin IgG on H2O2-induced endothelial cell adhesion molecules and chemokines expression. Methods IgG and H2O2 were added to endothelial cells and incubated for 2 h. The expressions of ICAM-1, VCAM-1, E-se-lectin and MCP-1 were detected by RT-PCR and real- -1, MIP-2) mRNA and protein expression; Further Western blot was used to detect H2O2-induced phosphorylation of p38, ERK1 / 2 and JNK1 / 2. Results H2O2 significantly induced the expression of ICAM-1, VCAM-1 and E-selectin, chemokines (MCP-1, CXCL-1 and MIP-2) And IgG can inhibit H2O2-induced phosphorylation of p38, JNK1 / 2 and ERK1 / 2. Conclusion The inhibitory effect of IgG on the expression of endothelial cell adhesion molecules and chemokines induced by H2O2 may be through the inhibition of the signal pathways of p38, JNK1 / 2 and ERK1 / 2, which may be one of the mechanisms by which IgG regulates the inflammation of endothelial cells.