Hypertension and Vascular Research Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva Israel and Internal Medicine Division Shaare Zedek Medical Center, Jerusalem, Israel.
Biochem Biophys Res Commun. 2018 Jun 12;500(4):944-951. doi: 10.1016/j.bbrc.2018.04.206. Epub 2018 May 2.
The pro-inflammatory vasoconstrictor Angiotensin II can cause endothelial dysfunction and is considered to be one of the mediators of atherosclerosis. Our former results demonstrated that polysaccharides derived from the red alga Porphyridium sp. attenuate inflammatory processes by interfering with tumor necrosis factor-alpha-induced inflammation, in human coronary artery endothelial cells. However, the anti-inflammatory effect of these polysaccharides on inflammation processes occurring under Angiotensin II stimulation is yet unknown. Herein, we studied the polysaccharide's anti-inflammatory effect by quantification of inflammatory markers in Angiotensin II- stimulated Human Coronary Artery Endothelial Cells following pre-treatment with polysaccharides. Inflammatory atherosclerotic pathways up-regulated by Angiotensin II, including adhesion molecule expression and nuclear factor kappa-light-chain-enhancer of activated B cells translocation, were significantly attenuated or diminished in cells pre-treated with the polysaccharides. In addition, the polysaccharides increased the antioxidant response elements activity through the nuclear factor-E2-related factor 2- antioxidant protection system. These polysaccharide's promising abilities may be considered as a basis for future use as a therapeutic agent aimed at improving vascular health by attenuation of the inflammatory atherosclerotic process.
促炎血管收缩素 Angiotensin II 可导致内皮功能障碍,被认为是动脉粥样硬化的介质之一。我们之前的研究结果表明,来源于红藻 Porphyridium sp. 的多糖通过干扰肿瘤坏死因子-α诱导的炎症来减轻炎症过程,在人冠状动脉内皮细胞中。然而,这些多糖在 Angiotensin II 刺激下发生的炎症过程中的抗炎作用尚不清楚。在此,我们通过在多糖预处理后定量测定 Angiotensin II 刺激的人冠状动脉内皮细胞中的炎症标志物来研究多糖的抗炎作用。Angiotensin II 上调的炎症性动脉粥样硬化途径,包括粘附分子表达和核因子 kappa-轻链增强子的 B 细胞易位,在经多糖预处理的细胞中明显减弱或减少。此外,多糖通过核因子-E2 相关因子 2-抗氧化保护系统增加抗氧化反应元件的活性。这些多糖的有希望的能力可以被认为是未来作为治疗剂的基础,旨在通过减轻炎症性动脉粥样硬化过程来改善血管健康。