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Protective Effects of Ferulic Acid on High Glucose-Induced Protein Glycation Lipid Peroxidation and Membrane Ion Pump Activity in Human Erythrocytes

机译:阿魏酸对高糖诱导的蛋白质糖基化脂质过氧化和人类红细胞膜离子泵活性的保护作用。

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摘要

Ferulic acid (FA) is the ubiquitous phytochemical phenolic derivative of cinnamic acid. Experimental studies in diabetic models demonstrate that FA possesses multiple mechanisms of action associated with anti-hyperglycemic activity. The mechanism by which FA prevents diabetes-associated vascular damages remains unknown. The aim of study was to investigate the protective effects of FA on protein glycation, lipid peroxidation, membrane ion pump activity, and phosphatidylserine exposure in high glucose-exposed human erythrocytes. Our results demonstrated that FA (10-100 μM) significantly reduced the levels of glycated hemoglobin (HbA1c) whereas 0.1-100 μM concentrations inhibited lipid peroxidation in erythrocytes exposed to 45 mM glucose. This was associated with increased glucose consumption. High glucose treatment also caused a significant reduction in Na+/K+-ATPase activity in the erythrocyte plasma membrane which could be reversed by FA. Furthermore, we found that FA (0.1-100 μM) prevented high glucose-induced phosphatidylserine exposure. These findings provide insights into a novel mechanism of FA for the prevention of vascular dysfunction associated with diabetes.
机译:阿魏酸(FA)是肉桂酸普遍存在的植物化学酚醛衍生物。在糖尿病模型中的实验研究表明,FA具有与抗高血糖活性相关的多种作用机制。 FA预防糖尿病相关血管损伤的机制尚不清楚。研究的目的是研究FA对高糖暴露的人红细胞中蛋白质糖基化,脂质过氧化,膜离子泵活性和磷脂酰丝氨酸暴露的保护作用。我们的结果表明,FA(10-100μM)显着降低了糖化血红蛋白(HbA1c)的水平,而0.1-100μM的浓度抑制了暴露于45 mM葡萄糖的红细胞的脂质过氧化。这与葡萄糖消耗增加有关。高葡萄糖处理还导致红细胞质膜Na + / K + -ATPase活性显着降低,而FA可以逆转该活性。此外,我们发现FA(0.1-100μM)可以防止高葡萄糖诱导的磷脂酰丝氨酸暴露。这些发现为FA预防与糖尿病相关的血管功能障碍的新机制提供了见识。

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