摘要
高血压、糖尿病、脂质代谢紊乱和肥胖常常簇集出现而形成代谢综合征，严重影响公众的健康水平。近年来，代谢性疾病的微炎症背景备受学者关注，微炎症状态与代谢性疾病的发生发展密切关联。肾素一血管紧张素系统（RAS），除了血流动力学调节作用外，在微炎症反应中也发挥重要的作用。阻断RAS，对代谢性疾病具有一定的保护作用。目前已证实，RAS主要通过血管紧张素转换酶一血管紧张素1I-ATl受体（ACE-AnglI-ATlR）轴和ACE2-Ang（1-7）-Mas轴发挥作用，这两条途径具有相反的生物学活性，后者对前者有拈抗作用。血管紧张素Ⅱ（AngII）由血管紧张素Ⅱ受体介导通过多种机制发挥致炎作用，而Ang（1-7）可以拮抗AngII，抑制炎症反应。本文就RAS参与微炎症反应的相关机制做一综述。
The cluster of hypertension, diabetes mellitus, dyslipidemia and body obesity, collectively referred to as the metabolic syndrome, is a common cause of atherosclerotic and cardiovascular diseases, and also one of the most serious threats to public health. Metabolic syndrome is closely related to micro-inflammation, which receives great attention in recent years. Besides the hemodynamic regulatory role, renin-angiotensin system （RAS） also plays an important role in micro-inflammation. Blockade of RAS could protect against the development of metabolic syndrome. It has been confirmed that RAS exerts its effects mainly through angiotensin converting enzyme（ACE）-angiotensin II （Ang Ⅱ）-angiotensin 1 receptor（AT1R） axis and ACE2-Ang（1-7）-Mas axis, and the two approaches have opposite biological activities. Angiotensin（Ang）Ⅱ could initiate inflammation through a variety of mechanisms by its receptors, but the Angl-7, as the antagonists to Ang Ⅱ, restrains the inflammation. In this paper, we reviewed the mechanism through which RAS is involved in micro-inflamrnntlcm
出处
《中华老年多器官疾病杂志》
2012年第2期146-149,共4页
Chinese Journal of Multiple Organ Diseases in the Elderly
