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目的:研究急性进展性脑梗死(APCI)患者外周血清可溶性CD40配体(sCD40L)水平及外周血单个核细胞(PB-MC)胞核核因子κB(NF-κB)p65表达率的变化。方法:采用前瞻性研究方法选择起病7d以内的99例APCI患者作为APCI组,选择同期急性脑梗死(ACI)患者及门诊查体的脑动脉硬化(CAS)患者各100例分别作为ACI组和CAS组;CAS组于查体时,APCI组及ACI组于入院时、病程第7天、第14天、第30天分别监测患者外周血清sCD40L及PBMC胞核NF-κBp65表达率的变化。结果:ACI组入院时外周血清sCD40L及PBMC胞核NF-κBp65表达率均明显高于CAS组(P<0.05),APCI组于入院时、病程第7天、第14天及第30天外周血清sCD40L及PBMC胞核NF-κBp65表达率均明显高于ACI组(P<0.05)。结论:CD40-CD40L信号通路及PB-MC胞核NF-κB表达的过度上调而介导的炎症、凋亡机制可能是APCI发生与发展的分子生物学机制之一。
Objective: To study the changes of soluble CD40 ligand (sCD40L) and the expression of nuclear factor kappa B (NF-κB) p65 in peripheral blood mononuclear cells (PBMCs) in acute progressive cerebral infarction (APCI) patients. Methods: A prospective study was conducted to select 99 patients with APCI within 7 days after onset as the APCI group. One hundred patients with cerebral arteriosclerosis (CAS) were enrolled as ACI group and CAS group. In the CAS group, APCI group and ACI group were monitored on the 7th, 14th, and 30th days of the course of disease. The changes of sCD40L and nuclear NF-κBp65 expression in peripheral blood mononuclear cells were detected in the CAS group. Results: The expression rates of sCD40L and NF-κBp65 in PBMC of ACI group were significantly higher than those of CAS group (P <0.05), and the APCI group was significantly higher on the admission day, the seventh day, the 14th day and the 30th day The expression rates of sCD40L and nuclear NF-κBp65 in PBMC were significantly higher than those in ACI group (P <0.05). Conclusion: Inflammatory and apoptosis mechanisms mediated by over-upregulation of CD40-CD40L signaling pathway and nuclear NF-κB in PB-MC may be one of the molecular mechanisms of APCI development and progression.