巨噬细胞β-arrestin-1对动脉粥样硬化的作用机制研究  

Mechanism of action of macrophageβ-arrestin-1 on atherosclerosis

作　　者：蒋恒波 杨红霞[2] Jiang Hengbo;Yang Hongxia(The Traditional Chinese Medical Hospital of Xintian County,Hunan Yongzhou 425000;Hunan Yongzhou Vocational and Technical College,Hunan Yongzhou 425100)

机构地区：[1]新田县中医医院,湖南永州425000 [2]湖南永州职业技术学院,湖南永州425100

出　　处：《中国社区医师》2021年第25期5-6,共2页Chinese Community Doctors

摘　　要：目的:探究巨噬细胞β-arrestin-1对动脉粥样硬化的作用机制。方法:选取实验小鼠,建立动脉粥样硬化小鼠模型,观察巨噬细胞β-arrestin-1的作用机制。结果:β-arrestin-1蛋白表达后,小鼠动脉粥样硬化程度更加严重,主动脉整体斑块面积增加。主动脉根部斑块面积增加,斑块的不稳定性增加。PNU282987激动α7nAChR后,动脉粥样硬化更加严重,主动脉整体斑块面积明显减少。并且斑块的稳定性增加,主动脉根部粥样斑块面积减少。对于多发性硬化小鼠模型,脊髓小胶质细胞β-arrestin-1明显增加。β-arrestin-1蛋白表达后,很大程度抑制了激动a7nAChR的作用。β-arrestin-1蛋白表达,影响PNU282987激动α7nAChR抑制NLRP3炎性小体作用。结论:巨噬细胞β-arrestin-1有抗动脉粥样硬化作用,并且介导α7nAChR,发挥抗动脉粥样硬化的作用。Objective:To explore the mechanism of action of macrophageβ-arrestin-1 on atherosclerosis.Methods:We selected experimental mice to establish atherosclerosis mouse model and observe the mechanism of action of macrophageβ-arrestin-1.Results:After the expression ofβ-arrestin-1 protein,the degree of atherosclerosis in mice was more serious,and the total area of aortic plaque increased.The plaque area and instability of aortic root increased.After PNU282987 activatingα7nAChR,atherosclerosis was more serious,significantly reducing the overall aortic plaque area.The stability of plaque increased and the area of atherosclerotic plaque decreased.In multiple sclerosis mouse model,spinal microgliaβ-arrestin-1 increased significantly.After the expression ofβ-arrestin-1 protein,the activation of activatingα7nAChR was inhibited to a great extent.The expression ofβ-arrestin-1 protein affected the effect of PNU282987 activatingα7nAChR inhibiting of NLRP3 inflammasome.Conclusion:Macrophageβ-arrestin-1 has anti atherosclerotic effect,and mediatesα7nAChR,playes the role of anti atherosclerosis.

关 键 词：巨噬细胞 β-arrestin-1 动脉粥样硬化 多发性硬化 作用机制 

分 类 号：R543.5[医药卫生—心血管疾病]