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本文引用的文献

1
Glucagon-like Peptide-1 Receptor Agonists and Cardiovascular Events: Class Effects versus Individual Patterns.胰高血糖素样肽-1 受体激动剂与心血管事件:类别效应与个体模式。
Trends Endocrinol Metab. 2018 Apr;29(4):238-248. doi: 10.1016/j.tem.2018.01.011. Epub 2018 Feb 17.
2
Cardiovascular Disease and Type 2 Diabetes: Has the Dawn of a New Era Arrived?心血管疾病与2型糖尿病:新时代已经来临了吗?
Diabetes Care. 2017 Jul;40(7):813-820. doi: 10.2337/dc16-2736.
3
Liraglutide, a GLP-1 receptor agonist, inhibits vascular smooth muscle cell proliferation by enhancing AMP-activated protein kinase and cell cycle regulation, and delays atherosclerosis in ApoE deficient mice.利拉鲁肽是一种胰高血糖素样肽-1(GLP-1)受体激动剂,它通过增强AMP激活的蛋白激酶和细胞周期调节来抑制血管平滑肌细胞增殖,并延缓载脂蛋白E缺乏小鼠的动脉粥样硬化进程。
Atherosclerosis. 2017 Jun;261:44-51. doi: 10.1016/j.atherosclerosis.2017.04.001. Epub 2017 Apr 7.
4
Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes.利拉鲁肽与2型糖尿病患者的心血管结局
N Engl J Med. 2016 Jul 28;375(4):311-22. doi: 10.1056/NEJMoa1603827. Epub 2016 Jun 13.
5
Anti-Inflammatory Effects of GLP-1-Based Therapies beyond Glucose Control.基于胰高血糖素样肽-1(GLP-1)的疗法在控制血糖之外的抗炎作用。
Mediators Inflamm. 2016;2016:3094642. doi: 10.1155/2016/3094642. Epub 2016 Mar 24.
6
Vascular Smooth Muscle Cells in Atherosclerosis.动脉粥样硬化中的血管平滑肌细胞
Circ Res. 2016 Feb 19;118(4):692-702. doi: 10.1161/CIRCRESAHA.115.306361.
7
A Randomized, Controlled Trial of 3.0 mg of Liraglutide in Weight Management.利拉鲁肽 3.0 毫克在体重管理中的随机、对照试验。
N Engl J Med. 2015 Jul 2;373(1):11-22. doi: 10.1056/NEJMoa1411892.
8
Atherosclerosis and the role of immune cells.动脉粥样硬化与免疫细胞的作用。
World J Clin Cases. 2015 Apr 16;3(4):345-52. doi: 10.12998/wjcc.v3.i4.345.
9
Physiology of proglucagon peptides: role of glucagon and GLP-1 in health and disease.胰高血糖素原肽的生理学:胰高血糖素和 GLP-1 在健康和疾病中的作用。
Physiol Rev. 2015 Apr;95(2):513-48. doi: 10.1152/physrev.00013.2014.
10
Di-(2-ethylhexyl) phthalate accelerates atherosclerosis in apolipoprotein E-deficient mice.邻苯二甲酸二(2-乙基己基)酯加速载脂蛋白E缺乏小鼠的动脉粥样硬化进程。
Arch Toxicol. 2016 Jan;90(1):181-90. doi: 10.1007/s00204-014-1377-5. Epub 2014 Oct 2.

胰高血糖素样肽-1 受体激动剂可降低二(2-乙基己基)邻苯二甲酸酯诱导的血管平滑肌细胞动脉粥样硬化过程。

Glucagon-like peptide-1 receptor agonist reduces di(2-ethylhexyl) phthalate-induced atherosclerotic processes in vascular smooth muscle cells.

机构信息

Department of Internal Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, South Korea.

出版信息

Physiol Res. 2020 Dec 22;69(6):1095-1102. doi: 10.33549/physiolres.934480. Epub 2020 Nov 2.

DOI:10.33549/physiolres.934480
PMID:33129247
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8549877/
Abstract

Glucagon-like peptide-1 receptor (GLP1R) agonist is an incretin hormone and regulates glucose metabolism. However, phthalates, known as endocrine disruptors, can interfere with hormone homeostasis. In the present study, we aimed to estimate the impact of GLP1R agonist on di(2 ethylhexyl) phthalate (DEHP)-induced atherosclerosis. For this purpose, the effects of GLP1R agonist on various atherogenesis-related cellular processes and pathways were assessed in vascular smooth muscle cells (VSMCs). DEHP-induced cell proliferation and migration were significantly decreased by GLP1R agonist in VSMCs. Protein levels of matrix metalloproteinase (MMP)-2 and MMP-9 were significantly decreased in cells exposed to GLP1R agonist, compared with DEHP-treated cells. Expression levels of intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 were also reduced in GLP1R agonist-treated cells. Similarly, DEHP-associated phosphorylation of protein kinase B and extracellular signal-regulated kinase 1/2 was decreased in GLP1R agonist-treated cells, compared with DEHP-treated cells. Our findings suggest that treatment with GLP1R agonist counteracts the activation of pathways related to atherosclerosis.

摘要

胰高血糖素样肽-1 受体 (GLP1R) 激动剂是一种肠促胰岛素激素,可调节葡萄糖代谢。然而,邻苯二甲酸酯作为内分泌干扰物,会干扰激素平衡。在本研究中,我们旨在评估 GLP1R 激动剂对邻苯二甲酸二(2-乙基己基)酯 (DEHP) 诱导的动脉粥样硬化的影响。为此,在血管平滑肌细胞 (VSMC) 中评估了 GLP1R 激动剂对各种动脉粥样硬化相关细胞过程和途径的影响。GLP1R 激动剂可显著降低 VSMC 中 DEHP 诱导的细胞增殖和迁移。与 DEHP 处理的细胞相比,GLP1R 激动剂处理的细胞中基质金属蛋白酶 (MMP)-2 和 MMP-9 的蛋白水平显著降低。细胞间黏附分子 1 和血管细胞黏附分子 1 的表达水平在 GLP1R 激动剂处理的细胞中也降低。同样,与 DEHP 处理的细胞相比,GLP1R 激动剂处理的细胞中蛋白激酶 B 和细胞外信号调节激酶 1/2 的磷酸化也减少。我们的研究结果表明,GLP1R 激动剂的治疗可拮抗与动脉粥样硬化相关的途径的激活。