【摘要】 目的:研究急性脑梗死患者血清miR-221表达的变化及其靶向炎症反应激活的作用。方法:选择2015年3月-2018年10月在本院诊断为急性脑梗死的56例患者作为脑梗死组,同期体检且一般资料匹配的40例健康志愿者作为对照组,检测血清miR-221、Toll样受体(TLR4)及核因子-κB(NF-κB)的表达及神经标志物、炎症因子的含量。结果:与对照组比较,脑梗死组患者的血清miR-221表达量及脑源性神经营养因子(BDNF)含量均明显降低,血清神经元特异性烯醇化酶(NSE)、S100B、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)含量及TLR4、NF-κB表达量均明显升高(P<0.05);经Pearson检验分析,脑梗死组患者miR-221的表达量与NSE、S100B、TNF-α、IL-1β、ICAM-1、VCAM-1含量及TLR4、NF-κB表达量均呈负相关,与BDNF含量呈正相关(P<0.05)。结论:血清miR-221表达的降低与急性脑梗死的发生及神经损伤的加重有关,靶向激活炎症反应是其可能的分子机制。更多还原

【Abstract】 Objective:To study the changes of serum miR-221 expression in patients with acute cerebral infarction and its role in targeting the activation of inflammatory response.Method:A total of 56 patients with acute cerebral infarction diagnosed in our hospital from March 2015 to October 2018 were selected as the cerebral infarction group,and 40 healthy volunteers matched with general data during the same period were selected as the control group.The expression of serum miR-221,toll like receptor 4(TLR4),nuclear factor-κB(NF-κB)and the contents of neurological markers and inflammatory factors were detected.Result:Compared with the control group,the expression of miR-221 and the content of brain-derived neurotrophic factor(BDNF)in serum of the cerebral infarction group were significantly decreased,and serum neuron-specific enolase(NSE),S100 B,tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1(VCAM-1)contents and TLR4,NF-κB expression significantly increased(P<0.05).Pearson test showed that the expression of miR-221 was negatively correlated with the contents of NSE,S100 B,TNF-α,IL-1β,ICAM-1,VCAM-1 and the expression of TLR4,NF-κB,and positively correlated with the levels of BDNF in patients with cerebral infarction(P<0.05).Conclusion:The decrease of serum miR-221 expression is related to the occurrence of acute cerebral infarction and the aggravation of nerve injury,targeted activation of inflammatory response is its possible molecular mechanism.更多还原