A20干预动脉粥样硬化炎症机制的研究
基本信息
结项摘要
动脉粥样硬化是一种慢性炎症过程，感染、氧化低密度脂蛋白（ox-LDL）、血管紧张素Ⅱ（AngⅡ）等使NF-κB等核转录因子过度活化触发炎症反应而参与动脉粥样硬化发生发展。介导炎症和先天免疫反应的受体Toll样受体4（TLR4）存在于血管内皮细胞、平滑肌细胞和单核细胞等，TLR4/NF-κB信号通路在动脉粥样硬化炎症机制中可能起重要作用。锌指蛋白A2 0是一种泛素调节酶，通过泛素化和去泛素化调节TLR4/NF-κB信号。本研究从离体和在体两方面，应用离体内皮细胞、平滑肌细胞、单核细胞及动脉段培养和在体动脉粥样硬化动物模型，通过质粒转染增强或干扰抑制A20表达等分子生物学手段，观察A20在血管炎症损伤反应过程中的表达规律，探讨A20对TLR4/NF-kB信号通路的调节作用和对动脉粥样硬化发生发展的影响，为直接控制炎症机制治疗动脉粥样硬化提供理论和实践依据。
项目摘要
项目成果
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数据更新时间：2023-05-31
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