医学
血管紧张素II
纤维化
炎症
心室重构
肾素-血管紧张素系统
内科学
内分泌学
心力衰竭
血压
高血压的病理生理学
醛固酮
心脏纤维化
心肌梗塞
心脏病学
血管紧张素受体
促炎细胞因子
血管紧张素Ⅱ受体1型
作者
Francisco Olivares-Silva,Nicole De Gregorio,Jenaro Espitia-Corredor,Claudio Espinoza,Raúl Vivar,David Silva,José Miguel Osorio,Sergio Lavandero,Concepción Peiró,Carlos F. Sánchez-Ferrer,Guillermo Díaz-Araya
标识
DOI:10.1016/j.bbadis.2021.166241
摘要
Despite the broad pharmacological arsenal to treat hypertension, chronic patients may develop irreversible cardiac remodeling and fibrosis. Angiotensin II, the main peptide responsible for the Renin-Angiotensin-Aldosterone-System, has been closely linked to cardiac remodeling, hypertrophy, fibrosis, and hypertension, and some of these effects are induced by inflammatory mediators. Resolvin-D1 (RvD1) elicits potent anti-inflammatory and pro-resolving effects in various pathological models. In this study, we aimed to examine whether RvD1 ameliorates cardiac remodeling and hypertension triggered by angiotensin II.Alzet® osmotic mini-pumps filled with angiotensin II (1.5 mg/kg/day) were implanted in male C57BL/6 J mice for 7 or 14 days. RvD1 (3 μg/kg/day, i.p) was administered one day after the surgery and during the complete infusion period. Blood pressure and myocardial functional parameters were assessed by echocardiography. At the end of the experimental procedure, blood and heart tissue were harvested, and plasma and histological parameters were studied. After 7 and 14 days, RvD1 reduced the increase of neutrophil and macrophage infiltration triggered by angiotensin II, and also reduced ICAM-1 and VCAM-1 expression levels. RvD1 also reduced cytokine plasma levels (IL-1β, TNF-α, IL-6, KC, MCP-1), cardiac hypertrophy, interstitial and perivascular fibrosis, and hypertension.This study unveils novel cardioprotective effects of RvD1 in angiotensin II-induced hypertension and cardiac remodeling by attenuating inflammation and provides insights into a potential clinical application.
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