摘要
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。
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.
出处
《中国生化药物杂志》
CAS
CSCD
北大核心
2012年第6期713-716,724,共5页
Chinese Journal of Biochemical Pharmaceutics
基金
福建省科技计划重点项目(2010Y0053)
国家自然科学基金资助项目(81270249)
福建省自然科学基金资助项目(2012J01415)
