蛋白酶激活受体-1在动脉粥样硬化中的作用及其机制研究  

Role of protease-activated receptor-1 in atherosclerosis and its mechanism

作　　者：宋伟 蔡海鹏 SONG Wei;CAI Haipeng(Depart-ment of Cardiovascular Medicine,Taizhou Central Hospital(Affiliated Hospital of Taizhou University),Taizhou 318000,China.)

机构地区：[1]台州市中心医院(台州学院附属医院)心血管内科,浙江台州318000

出　　处：《全科医学临床与教育》2023年第3期203-206,F0002,共5页Clinical Education of General Practice

基　　金：台州市第二批社会发展科技计划项目(20ywb47)。

摘　　要：目的分析蛋白酶激活受体-1(PAR-1)在动脉粥样硬化中的作用及其机制研究。方法选取40只ApoE(-/-)小鼠,将40只小鼠随机分为对照组、模型组、PAR-1模拟物组、PAR-1抑制剂组,每组10只。比较各组的PAR-1相对表达量、小鼠斑块泡沫细胞占比、斑块脂质核心面积百分比、丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、胆固醇(TC)、甘油三酯(TG)水平、MAPKs、NF-κB信号通路蛋白。结果PAR-1抑制剂组的PAR-1相对表达量低于PAR-1模拟物组、模型组,高于对照组,差异均有统计学意义(t分别=10.63、8.49、-8.49,P均<0.05);PAR-1抑制剂组的斑块泡沫细胞占比、斑块脂质核心面积百分比低于PAR-1模拟物组、模型组,差异均有统计学意义(t分别=56.21、42.76;20.65、21.72,P均<0.05);PAR-1抑制剂组的ALT、AST、TC、TG低于PAR-1模拟物组、模型组,高于对照组,差异均有统计学意义(t分别=16.84、5.18、-0.99;11.66、5.24、-1.73;31.30、18.85、-52.98;10.10、2.39、-12.38,P均<0.05);PAR-1抑制剂组的MAPKs、NF-κB蛋白低于PAR-1模拟物组、模型组,高于对照组,差异均有统计学意义(t分别=12.89、8.49、-2.86;8.43、4.79、-3.43,P均<0.05)。结论抑制PAR-1表达,可以使小鼠斑块泡沫细胞占比、斑块脂质核心面积百分比降低,改善小鼠血脂水平,其机制可能与MAPKs/NF-κB信号通路被抑制有关。Objective To investigate the role of protease-activated receptor-1(PAR-1)in atherosclerosis and its mechanism.Methods Forty ApoE(-/-)mice were selected and randomly divided into control group,model group,PAR-1 mock group,and PAR-1 inhibitor group,with 10 mice in each group.Relative expression of PAR-1,the proportion of plaque foam cells,the percentage of plaque lipid core area,ALT,AST,TC,TG levels,and MAPKs/NF-κB signaling pro⁃teins were compared.Results The relative amount of PAR-1 expression in the PAR-1 inhibitor group was lower than that in the PAR-1 mock group and the model group,while higher than that in the control group(t=10.63,8.49,-8.49,P<0.05).The proportion of plaque foam cells,the percentage of plaque lipid core area in the PAR-1 inhibitor group were lower than those in the PAR-1 mock group and the model group(t=56.21,42.76,20.65,21.72,P<0.05).The ALT,AST,TC,and TG of the PAR-1 inhibitor group were lower than those of the PAR-1 mock group and the model group,while higher than that in the control group(t=16.84,5.18,-0.99,11.66,5.24,-1.73,31.30,18.85,-52.98,10.10,2.39,-12.38,P<0.05).The MAPKs and NF-κB proteins in the PAR-1 inhibitor group were lower than those in the PAR-1 mock group and the model group,while higher than that in the control group(t=12.89,8.49,-2.86,8.43,4.79,-3.43,P<0.05).Conclusion Inpressed expression of PAR-1 can reduce the plaque foam cell proportion,per⁃centage of plaque lipid core area,and improve in⁃flammatory cytokine levels,Its mechanism probably relate to the restrain to MAPKs/NF-κB signaling.

关 键 词：动脉粥样硬化 蛋白酶激活受体 信号通路 机制研究 

分 类 号：R543.5[医药卫生—心血管疾病]