Hyperglycemia triggers metabolic and inflammatory responses, which lead to vascular inflammation and consequently induce microvascular and/or macrovascular diabetic complications. 5-bromo-3,4-dihydroxybenzaldehyde (BDB), a marine red algae-derived bromophenol compound, is found to have diverse bioactivities, including the effect of anti-inflammation and anti-diabetes, though the mechanism of which is still unclear. To evaluate the anti-vasculopathy of BDB and explore the possible mechanism involved. Firstly, MTT assay was used to optimize the treatment concentration of glucose and BDB with HUVECs. Subsequently, we adopted two concentrations of BDB (50 µM and 100 µM) to verify the protective effect of BDB on vascular model, which was established by HUVECs from high glucose (30 mM)-induced damage. The cell migration and tube formation were used to evaluate the function of HUVECS. Moreover, the related mechanisms were analyzed by assays for flow cytometry, ELISA, qPCR, intracellular ROS and western blot. The present study demonstrated that BDB could protect endothelial cells from apoptosis caused by high glucose treatment. BDB also significantly reduced the secretion of inflammatory cytokines, such as TNF-α, IL-1β and IL-6, induced by high glucose, which was also in agreement to the decrease of p65 protein expression and activities of NF-ĸB regulated by BDB. The reactive oxygen species (ROS) production and phosphorylation of 38 protein expression were also down-regulated by BDB compared to high glucose alone treatment. Furthermore, BDB reserved the endothelial cells functions of migration and tube formation under high glucose condition, which suggested that BDB could be a potential candidate in treating vascular inflammation induced by hyperglycemia.

中文翻译：

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5-溴-3,4-二羟基苯甲醛可减轻高葡萄糖引起的内皮细胞损伤。


高血糖会引发代谢和炎症反应，从而导致血管炎症，从而诱发微血管和/或大血管糖尿病并发症。 5-溴-3,4-二羟基苯甲醛（BDB）是一种源自海洋红藻的溴酚化合物，被发现具有多种生物活性，包括抗炎和抗糖尿病作用，但其机制仍不清楚。评价BDB的抗血管病变作用并探讨其可能的机制。首先，采用MTT法优化葡萄糖和BDB对HUVECs的处理浓度。随后，我们采用两种浓度的BDB（50 µM和100 µM）来验证BDB对HUVEC建立的高糖（30 mM）损伤血管模型的保护作用。细胞迁移和管形成用于评估HUVECS的功能。此外，通过流式细胞术、ELISA、qPCR、细胞内ROS和蛋白质印迹分析相关机制。本研究表明，BDB 可以保护内皮细胞免受高糖处理引起的细胞凋亡。 BDB还显着减少高糖诱导的炎症细胞因子的分泌，如TNF-α、IL-1β和IL-6，这也与BDB调节的p65蛋白表达和NF-ĸB活性的降低相一致。 。与单独高葡萄糖处理相比，BDB 也下调了活性氧 (ROS) 的产生和 38 种蛋白表达的磷酸化。此外，BDB保留了高血糖条件下内皮细胞的迁移和管形成功能，这表明BDB可能是治疗高血糖引起的血管炎症的潜在候选者。