三甲胺-N-氧化物协同RAS诱导动脉粥样硬化发展机制研究  

Study on the development mechanism of action of TMAO cooperating RAS system to induce atherosclerosis

作　　者：郑平 王东鹏 ZHENG Ping;WANG Dongpeng(Fuzhou Hospita lof Traditional Chinese Medicine Affiliated to Fujian University of Traditional Chinese Medicine,Fuzhou,Fujian 350004,China)

机构地区：[1]福建中医药大学附属福州中医院,福州350004

出　　处：《福建医药杂志》2023年第1期96-102,F0003,共8页Fujian Medical Journal

基　　金：福州市市级科技计划项目(2019-SZ-29)。

摘　　要：目的 探究三甲胺-N-氧化物(TMAO)与肾素-血管紧张素系统(RAS)在人脐静脉内皮细胞(HUVECs)炎症中的关系及作用机制。方法 采用分子克隆技术,构建血管紧张素Ⅱ(AngⅡ)过表达和敲减的HUVECs;TMAO干预上述HUVECs后,检测细胞中炎症因子及细胞增殖、迁移、血管形成能力,并分析细胞中RAS重要组分的表达水平。结果 成功构建了AngⅡ过表达和敲减的HUVECs;AngⅡ过表达促进TMAO调节HUVECs炎症,抑制HUVECs增殖,抑制HUVECs迁移能力,抑制HUVECs血管形成,促进细胞中RAS组分AGT、ACE、AngⅡ、ATR的表达;敲减AngⅡ抑制TMAO调节HUVECs炎症,促进HUVECs增殖,促进HUVECs迁移能力,促进HUVECs细胞的血管形成,抑制细胞中RAS组分AGT、ACE、AngⅡ、ATR的表达。结论 TMAO能够协同RAS诱导HUVECs炎症。Objective To explore the relationship and mechanism of TMAO and RAS in HUVECs inflammation.Methods Molecular cloning technology was used to construct overexpression and knockdown HUVECs of AngⅡ.After TMAO interfering with HUVECs, the inflammatory factors in cells, the ability of cell proliferation, and migration and angiogenesis were detected, and the expression level of RAS important components in cells was analyzed.Results Overexpression and knockdown HUVECs of AngⅡwere successfully constructed.Overexpression of AngⅡpromoted TMAO to regulate HUVECs inflammation, inhibited HUVECs proliferation, inhibited HUVECs migration ability, inhibited HUVECs angiogenesis, promoted the expression of RAS components AGT, ACE, AngⅡ, and ATR in cells.Knockdown of AngⅡinhibited TMAO to regulate HUVECs inflammation, promoted HUVECs proliferation, promoted HUVECs migration ability, promoted HUVECs angiogenesis, and inhibited the expression of RAS components AGT, ACE, AngⅡ, and ATR in cells.Conclusion TMAO can cooperate with RAS to induce HUVECs inflammation.

关 键 词：三甲胺-N-氧化物 RAS系统 人脐静脉内皮细胞 血管紧张素Ⅱ 

分 类 号：R543.5[医药卫生—心血管疾病]