摘要
在过去的数十年里,大麻体系(包括合成的和内源性的大麻素受体激动剂,他们的受体和降解酶)被证明在动脉粥样硬化和急性心血管疾病中诱导了强大的免疫调节活性。与传统的报道的其他大麻素受体不同,2型大麻素受体(CB2)选择性激活起着抗炎性和动脉粥样硬化血管和下游缺血周边器官中的保护作用。CB2是一类跨膜受体能够触发人类和动脉硬化动物模型心脏、免疫、血管细胞保护性的细胞内通路。考虑到基础研究数据,药物激活CB2在循环或者外周靶细胞的功能,可能是一个抵御动脉硬化的有前景的方法。本综述更新了在动脉粥样硬化和急性缺血性事件不同CB2-触发的通路中的临床前研究的证据。
关键词: 动脉硬化,大麻素受体,2型大麻素受体,缺血/再灌注损伤,缺血性中风。
Current Medicinal Chemistry
Title:Cannabinoid Receptor Type 2 Activation in Atherosclerosis and Acute Cardiovascular Diseases
Volume: 21 Issue: 35
Author(s): Federico Carbone, Francois Mach, Nicolas Vuilleumier and Fabrizio Montecucco
Affiliation:
关键词: 动脉硬化,大麻素受体,2型大麻素受体,缺血/再灌注损伤,缺血性中风。
摘要: In the last decades, the cannabinoid system (comprising synthetic and endogenous cannabinoid agonists and antagonists, their receptors and degrading enzymes) has been shown to induce potent immunomodulatory activities in atherogenesis and acute ischemic complications. Different from the other cannabinoid receptors in which controversial results are reported, the selective activation of the cannabinoid receptor type 2 (CB2) has been shown to play antiinflammatory and protective actions within atherosclerotic vessels and downstream ischemic peripheral organs. CB2 is a transmembrane receptor that triggers protective intracellular pathways in cardiac, immune and vascular cells in both human and animal models of atherosclerosis. Considering basic research data, medications activating CB2 function in the circulation or peripheral target organs might be a promising approach against atherogenesis. This review updates evidence from preclinical studies on different CB2-triggered pathways in atherosclerosis and acute ischemic events.
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Cite this article as:
Carbone Federico, Mach Francois, Vuilleumier Nicolas and Montecucco Fabrizio, Cannabinoid Receptor Type 2 Activation in Atherosclerosis and Acute Cardiovascular Diseases, Current Medicinal Chemistry 2014; 21 (35) . https://dx.doi.org/10.2174/0929867321666140915141332
DOI https://dx.doi.org/10.2174/0929867321666140915141332 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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