趋化因子CXCL10在心肌细胞及巨噬细胞中的表达机制

目的探讨心肌缺血-再灌注损伤中趋化因子CXCL10的产生机制。方法分别用LPS、H2O2、Ca2+载体A23187刺激原代培养的心肌细胞、骨髓来源的巨噬细胞或二者混合培养的共培养系统后,ELISA检测培养基上清中的趋化因子CXCL10和促炎性细胞因子IL-1β、IL-6、TNF-α的含量,观察其表达动力学。结果①大剂量(10μg/mL)的LPS刺激心肌细胞主要产生趋化因子CXCL10;刺激骨髓来源巨噬细胞主要产生促炎性细胞因子IL-1β、IL-6、TNF-α。②H2 O2、Ca2+通道激活剂并不能使产生趋化因子CXCL10或IL-1β、IL-6、TNF-α这些促炎性细胞因子。③骨髓来源的巨噬细胞促进心肌细胞表达趋化因子CXCL10;心肌细胞促进骨髓来源的巨噬细胞表达IL-6、TNF-α,但抑制IL-1β的表达。结论心肌细胞是心肌缺血-再灌注损伤中CXCL10潜在的细胞来源;CXCL10的表达,主要依赖于TLR4的激活。

Mechanism of CXCL10 expression in cardiac myocytes and bone marrow-derived macrophages

Objective To investigate the mechanism of CXCL10 expression during myocardial ischemia-reperfu-sion injury.Methods To stimulate cardiac myocytes,bone marrow-derived macrophages（BMMs） and co-culture system with LPS,H2 O2 or calcium ionophore A23187 respectively,and then test the CXCL10,IL-1β,IL-6,TNF-α levels in the supernant of medium by ELISA.Results ①High dose（10 μg /mL） LPS could induce cardiac myocytes to express CXCL10 as well as BMMs to produce IL-1β,IL-6,TNF-α.②H2 O2,calcium ionophore A23187 failed to induce CXCL10 expression or IL-1β,IL-6,TNF-α expression,either on cardiac myocytes or on BMMs.③BMMs promote CXCL10 induction of cardiac myocytes,while cardiac myocytes promote IL-6 and TNF-α induction of BMMs.Oppositely,the IL-1β induction of BMMs was inhibited by cardiac myocytes in this research.Conclusion Cardiac myocytes could be the potential cellular resource during myocardial ischemia-reperfusion injury.It is mainly the activation of TLR4 that cause CXCL10 expression.