Laboratorio de Metabolismo I, Departamento de Fisiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Ciudad de México 07738, Mexico.
Laboratorio de Neurobiología, Departamento de Fisiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Ciudad de México 07738, Mexico.
Nutrients. 2022 Mar 31;14(7):1464. doi: 10.3390/nu14071464.
C-phycocyanin (CPC) is an antihypertensive that is not still wholly pharmacologically described. The aim of this study was to evaluate whether CPC counteracts endothelial dysfunction as an antihypertensive mechanism in rats with 5/6 nephrectomy (NFx) as a chronic kidney disease (CKD) model. Twenty-four male Wistar rats were divided into four groups: sham control, sham-treated with CPC (100 mg/Kg/d), NFx, and NFx treated with CPC. Blood pressure was measured each week, and renal function evaluated at the end of the treatment. Afterward, animals were euthanized, and their thoracic aortas were analyzed for endothelium functional test, oxidative stress, and NO production. 5/6 Nephrectomy caused hypertension increasing lipid peroxidation and ROS production, overexpression of inducible nitric oxide synthase (iNOS), reduction in the first-line antioxidant enzymes activities, and reduced-glutathione (GSH) with a down-expression of eNOS. The vasomotor response reduced endothelium-dependent vasodilation in aorta segments exposed to acetylcholine and sodium nitroprusside. However, the treatment with CPC prevented hypertension by reducing oxidative stress, NO system disturbance, and endothelial dysfunction. The CPC treatment did not prevent CKD-caused disturbance in the antioxidant enzymes activities. Therefore, CPC exhibited an antihypertensive activity while avoiding endothelial dysfunction.
藻蓝蛋白（CPC）是一种具有降压作用但尚未完全阐明其药理学作用的物质。本研究旨在评估 CPC 是否可通过拮抗内皮功能障碍来发挥降压作用，从而作为一种治疗 5/6 肾切除（NFx）大鼠慢性肾病（CKD）模型的机制。将 24 只雄性 Wistar 大鼠分为四组：假手术对照组、假手术 CPC 治疗组（100mg/Kg/d）、NFx 组和 NFx+CPC 治疗组。每周测量血压，治疗结束时评估肾功能。之后处死动物，分析其胸主动脉以进行内皮功能测试、氧化应激和 NO 生成分析。5/6 肾切除导致高血压，增加脂质过氧化和 ROS 生成，诱导型一氧化氮合酶（iNOS）过度表达，一线抗氧化酶活性降低，还原型谷胱甘肽（GSH）减少，内皮型一氧化氮合酶（eNOS）表达下调。暴露于乙酰胆碱和硝普钠的主动脉段的血管舒缩反应降低，表明内皮依赖性血管舒张功能受损。然而，CPC 治疗可通过减轻氧化应激、NO 系统紊乱和内皮功能障碍来预防高血压。CPC 治疗并不能预防 CKD 引起的抗氧化酶活性紊乱。因此，CPC 表现出降压活性，同时避免了内皮功能障碍。
