BACKGROUND Ticagrelor and clopidogrel, P2Y12 receptor antagonists, can prevent thrombotic events and are used to treat cardiovascular diseases such as acute coronary syndrome and chronic obstructive pulmonary disease, in which inflammation is involved. Moreover, NF-B is the central regulator of inflammation. Thus, we suspected that ticagrelor and clopidogrel are involved in the regulation of the NF-ΚB signaling pathway. METHODS After human umbilical vein endothelial cells (HUVECs) were cultured with ticagrelor or clopidogrel and given lipopolysaccharide (LPS) and CD14, the mRNA levels of related inflammatory factors, the protein level and subcellular localization of molecules in the NF-ΚB signaling pathway, cell viability, apoptosis and the cell cycle, cell migration, and vascular formation were detected using quantitative polymerase chain reaction (qPCR), western blotting and immunofluorescence assay, CCK-8, flow cytometry, transwell assay, and matrigel, respectively. All data was expressed as the mean ± S.D. The statistical significance of data was assessed by an unpaired two-tailed t-test. RESULTS Ticagrelor and clopidogrel can inhibit the degradation of IKBα and phosphorylation of p65, prevent p65 from entering the nucleus, reduce the production of TNFα, IL-1, IL-8, IL-6 and IL-2, and alleviate the decrease in cell viability, cell migration and angiogenesis, the changes of cell cycle and apoptosis induced by LPS. CONCLUSIONS Ticagrelor and clopidogrel alleviate cellular dysfunction through suppressing NF-ΚB signaling pathway.

中文翻译：

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替卡格雷和氯吡格雷抑制NF-κB信号通路，减轻LPS诱导的静脉内皮细胞功能障碍。

背景技术替卡格雷和P2Y12受体拮抗剂氯吡格雷可预防血栓形成事件，并用于治疗涉及炎症的心血管疾病，例如急性冠状动脉综合征和慢性阻塞性肺疾病。此外，NF-B是炎症的中央调节剂。因此，我们怀疑替卡格雷和氯吡格雷参与了NF-κB信号通路的调控。方法用替卡格雷或氯吡格雷培养人脐静脉内皮细胞（HUVECs）并给予脂多糖（LPS）和CD14后，相关炎症因子的mRNA水平，蛋白水平和NF-κB信号通路中分子的亚细胞定位，细胞活力，细胞凋亡和细胞周期，细胞迁移，分别使用定量聚合酶链反应（qPCR），western印迹和免疫荧光测定，CCK-8，流式细胞术，transwell测定和matrigel检测血管形成。所有数据均以平均值±SD表示。数据的统计学显着性通过不成对的两尾t检验进行评估。结果替卡格雷和氯吡格雷可抑制IKBα降解和p65磷酸化，防止p65进入细胞核，减少TNFα，IL-1，IL-8，IL-6和IL-2的产生，并减轻细胞的减少脂多糖诱导的细胞活力，细胞迁移和血管生成，细胞周期变化和凋亡。结论替卡格雷和氯吡格雷可通过抑制NF-κB信号通路减轻细胞功能障碍。Transwell分析法和Matrigel。所有数据均表示为平均值±SD。数据的统计学显着性通过不成对的两尾t检验进行评估。结果替卡格雷和氯吡格雷可抑制IKBα降解和p65磷酸化，防止p65进入细胞核，减少TNFα，IL-1，IL-8，IL-6和IL-2的产生，并减轻细胞的减少脂多糖诱导的细胞活力，细胞迁移和血管生成，细胞周期变化和凋亡。结论替卡格雷和氯吡格雷可通过抑制NF-κB信号通路减轻细胞功能障碍。Transwell分析法和Matrigel。所有数据均表示为平均值±SD。数据的统计学显着性通过不成对的两尾t检验进行评估。结果替卡格雷和氯吡格雷可抑制IKBα降解和p65磷酸化，防止p65进入细胞核，减少TNFα，IL-1，IL-8，IL-6和IL-2的产生，并减轻细胞的减少脂多糖诱导的细胞活力，细胞迁移和血管生成，细胞周期变化和凋亡。结论替卡格雷和氯吡格雷可通过抑制NF-κB信号通路减轻细胞功能障碍。结果替卡格雷和氯吡格雷可抑制IKBα降解和p65磷酸化，防止p65进入细胞核，减少TNFα，IL-1，IL-8，IL-6和IL-2的产生，并减轻细胞的减少脂多糖诱导的细胞活力，细胞迁移和血管生成，细胞周期变化和凋亡。结论替卡格雷和氯吡格雷可通过抑制NF-κB信号通路减轻细胞功能障碍。结果替卡格雷和氯吡格雷可抑制IKBα降解和p65磷酸化，防止p65进入细胞核，减少TNFα，IL-1，IL-8，IL-6和IL-2的产生，并减轻细胞的减少脂多糖诱导的细胞活力，细胞迁移和血管生成，细胞周期变化和凋亡。结论替卡格雷和氯吡格雷可通过抑制NF-κB信号通路减轻细胞功能障碍。