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目的探讨Toll样受体(Toll-like receptor,TLR)介导丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)信号转导在体外对急性心肌梗塞(acute myocardial infarction,AMI)患者树突状细胞(dendritic cell,DC)的功能影响。方法将去年我院住院患者分3组:AMI组、稳定性心绞痛(stable pectoris,SP)组及正常对照组,各自从外周血中体外培养DC,各组DC分别应用流式细胞仪检测细胞表面TLR及CD80水平,RT-PCR检测TLR的mRNA水平,免疫印迹法检测MAPK家族中p38及JNK水平;HSP60刺激各组DC后分别应用ELISA法检测IL-6及TNF-α水平。结果 AMI组中DC表达TLR及MAPK家族水平、成熟标记物CD80水平、HSP60刺激后IL-6及TNF-α水平均明显升高(P<0.01)。结论 TLR介导MAPK信号转导参与AMI患者DC的活化过程。
Objective To investigate the effect of Toll-like receptor (TLR) -mediated mitogen-activated protein kinase (MAPK) signal transduction on dendrites in patients with acute myocardial infarction (AMI) Functional effects of dendritic cells (DCs). Methods The hospitalized patients in our hospital were divided into 3 groups: AMI group, stable pectoris group and normal control group. DCs were cultured from peripheral blood in vitro respectively. Flow cytometry was used to detect the cell surface TLR and CD80 levels were determined. The level of TLR mRNA was detected by RT-PCR. The levels of p38 and JNK in MAPK were detected by Western blotting. The levels of IL-6 and TNF-α were detected by ELISA after HSP60 stimulation. Results The levels of TLR and MAPK in AMI group were significantly higher than those in AMI group (P <0.01). The level of CD80 in mature AMI cells was significantly increased after stimulated with HSP60 (P <0.01). Conclusion TLR-mediated MAPK signaling is involved in the activation of DC in patients with AMI.