【摘要】 目的 本研究旨在探讨载脂蛋白C3(APOC3)对血管内皮细胞连接黏附分子-1(JAM-1)表达的调控作用，揭示其在动脉粥样硬化（AS）起始阶段中的潜在新机制。方法 在细胞层面，以人脐静脉内皮细胞（HUVECs）为模型，采用不同浓度（1～100μg/ml）的APOC3进行处理。在组织层面，建立小鼠主动脉培养模型，并同样给予APOC3干预。分别采用实时荧光定量聚合酶链反应（RT-qPCR）和免疫荧光技术检测HUVECs中JAM-1在基因和蛋白水平的表达变化；采用免疫组织化学技术观察小鼠主动脉组织JAM-1的蛋白表达与定位。结果 实验结果 表明，APOC3能够以浓度依赖性的方式显著促进HUVECs中JAM-1的mRNA和蛋白表达。在小鼠主动脉组织中，APOC3处理同样导致JAM-1蛋白表达显著上调，免疫组织化学定量分析显示其在内膜层的阳性表达面积和光密度值均明显增加。结论 APOC3能够显著诱导血管内皮细胞JAM-1的表达上调。APOC3-JAM-1轴通过促进细胞黏附，在AS早期的炎症反应及细胞趋化、渗出过程中可能发挥关键作用。更多还原

【Abstract】 Objective To explore the regulatory effect of Apolipoprotein C3(APOC3) on the expression of junction adhesion molecule-1(JAM-1) in vascular endothelial cells, thereby revealing its potential new mechanism in the initiation stage of atherosclerosis(AS). Methods At the cellular level, human umbilical vein endothelial cells(HUVECs) were used as a model and treated with APOC3 at different concentrations(1 ～100 μg/ml). At the organizational level, a mouse aortic culture model was established and APOC3 intervention was also administered.The expression changes of JAM-1 at the gene and protein levels in HUVECs were detected by qRT-PCR and immunofluorescence techniques respectively. The protein expression and localization of JAM-1 in the aortic tissue of mice were observed by immunohistochemical technique. Results The experimental results show that APOC3 can significantly promote the mRNA and protein expression of JAM-1 in HUVECs in a concentration-dependent manner. In the aortic tissue of mice, APOC3 treatment also led to a significant upregulation of JAM-1 protein expression. Immunohistochemical quantitative analysis showed that both the positive expression area and the optical density value in the intima layer increased significantly. Conclusions APOC3 promotes the upregulation of JAM-1 expression, which participate in leukocyte chemotaxis and endothelial exudation. This mechanism plays an important role in the pathogenesis of atherosclerosis, suggesting that APOC3 has potential as a novel therapeutic target for the prevention and treatment of cardiovascular diseases.更多还原