乔松素对心肌缺血再灌注后血管收缩功能的影响机制研究  

Study on the Mechanism of the Effect of Pinocembrin on Vasoconstriction after Myocardial Ischemia Reperfusion

作　　者：张弘 刘宗军[1] 刘颖 郜俊清[1] Zhang Hong;Liu Zongjun;Liu Ying;Gao Junqing(Department of Cardiology,Putuo Hospital of Shanghai University ofTraditional Chinese Medicine,Shanghai 200062,China)

机构地区：[1]上海中医药大学附属普陀医院心血管内科,上海200062

出　　处：《甘肃科学学报》2022年第1期40-47,89,共9页Journal of Gansu Sciences

基　　金：国家自然科学基金(81774076);上海中医药大学附属普陀医院院级培英人才计划“中药单体与微循环障碍的机制研究”(2016013B)。

摘　　要：揭示乔松素对心肌缺血再灌注后血管收缩功能影响的潜在机制。培养大鼠主动脉平滑肌细胞(VSMC),通过PDTC介导ETB受体增加,分为对照组、模型组、乔松素组(高、中、低剂量)。通过分子水平与蛋白水平检测分析血管内皮相关因子ETB、AT1R、BAX、NF-κB p65、ERK的表达,并通过对各实验组别细胞凋亡率、细胞存活率、细胞迁移数等分析研究其在细胞水平的变化情况。结果显示:乔松素高剂量组细胞凋亡率显著低于模型组与其他乔松素组(P<0.05);乔松素高剂量组细胞存活率与细胞迁移数显著高于模型组与其他乔松素组(P<0.05);乔松素高剂量组ETB、AT1R、BAX、NF-κB p65、ERK在mRNA水平和蛋白表达量方面显著低于模型组与其他乔松素组(P<0.05);在血液、脑组织和肝组织中模型组ROS表达量显著高于对照组及其他乔松素组(P<0.05)。研究表明乔松素可能通过抑制血管内皮相关因子ETB、AT1R、BAX、NF-κB p65、ERK的表达使得平滑肌细胞引起的血管收缩能力减弱。The purpose of this paper is to reveal the potential mechanism of the effect of pinocembrin on vasoconstriction after myocardial ischemia reperfusion.It cultured rat aortic VSMC and ETB receptors were increased by PDTC.The cells were divided into control group,model group and pinocembrin group(high,medium and low doses).The expression of ETB,AT1R,BAX,NF-κB p65 and ERK were detected at molecular level and protein level,and the changes of these factors at cell level were studied by cell apoptosis,cell survival rate and cell migration analysis in each experimental group.The apoptotic rate of the pinocembrin high-dose group was significantly lower than that of the model group and other groups(P<0.05);the cell survival rate and cell migration rate of this group were significantly higher than that of the model group and other groups(P<0.05);the levels of ETB,AT1R,BAX,NF-κB p65 and ERK in this high-dose group were significantly higher than those in the model group and other groups(P<0.05).The expression of ROS in blood,brain and liver tissue of model group was significantly higher than that of control group and EA group(P<0.05).Therefore,Pinocembrin may decrease the vasoconstrictive ability of VSMC by inhibiting the expression of ETB,AT1R,BAX,NF-κB p65 and ERK.

关 键 词：乔松素 血管内皮因子 血管平滑肌细胞 吡咯烷二硫代氨基甲酸酯 冠脉微循环 

分 类 号：R737.14[医药卫生—肿瘤]