急性脑梗死患者外周血单核细胞TLR4的表达与TNF-α、IL-6的相关性研究

Study on the correlation between the expression of TLR4 in peripheral blood mononuclear cells and TNF-α,IL-6 in patients with acute cerebral infarction

目的探讨急性脑梗死(ACI)患者外周血单核细胞Toll样受体4(TLR4)表达及其与肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)浓度的相关性。方法将2017年2月至2018年2月延安大学附属医院收治的54例发病3 d ACI患者作为ACI组,选取同期60例动脉粥样硬化患者作为动脉硬化组,另外选取同期在本院接受健康体检的58例身体健康体检者作为对照组,所有患者接受生化检验,观察三组研究对象TLR4mRNA在外周血单核细胞TLR4中的表达以及IL-6和TNF-α水平。结果ACI组TLR4mRNA表达以及IL-6和TNF-α水平均高于动脉硬化组和对照组,差异有统计学意义(P<0.05);同时ACI患者的TLR4mRNA表达和典型炎症因子IL-6和TNF-α呈正相关(P<0.05)。结论外周血单核细胞TLR4参与了ACI疾病炎性损伤的过程,通过调节TLR4的表达,促进IL-6、TNF-α等典型炎症因子的浓度上升,从而加速脑梗死的炎性损伤。

Objective To investigate the expression of Toll-like receptor 4(TLR4)on peripheral blood monocytes in patients with acute cerebral infarction(ACI)and its correlation with the concentration of tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6).Methods 54 patients with 3-day onset ACI admitted to the Affiliated Hospital of Yan’an University from February 2017 to February 2018 as the acute cerebral infarction group,and 60 patients with atherosclerosis during the same period were selected as the arteriosclerosis group.Fifty-eight healthy subjects who received physical examination in our hospital served as the control group.All patients received biochemical tests to observe the expression of TLR4 mRNA in peripheral blood mononuclear cells TLR4 and the levels of IL-6 and TNF-αin the three groups of subjects.Results The TLR4 mRNA expression and IL-6 and TNF-αlevels in the Aci group were higher than those in the arteriosclerosis group and the control group,and the difference was statistically significant(P<0.05).At the same time,the TLR4 mRNA expression and the typical inflammatory factors IL-6 and TNF in ACI patients-αwas positively correlated(P<0.05).Conclusion Peripheral blood mononuclear cells TLR4 participates in the inflammatory injury process of ACI disease.By regulating the expression of TLR4,it promotes the increase of the concentration of typical inflammatory factors such as IL-6 and TNF-α,thereby accelerating the inflammatory injury of cerebral infarction.