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-Bromo-3,4-dihydroxybenzaldehyde 可减轻高葡萄糖诱导的损伤导致的内皮细胞损伤。

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）是一种海洋红藻衍生的溴酚化合物，被发现具有多种生物活性，包括抗炎和抗糖尿病的作用，但其机制尚不清楚。评价 BDB 的抗血管病变作用并探讨其可能的作用机制。首先，MTT 法用于优化 HUVECs 对葡萄糖和 BDB 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 对血管模型的保护作用，该模型是由 HUVECs 建立的免受高糖（30 mM）诱导的损伤。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、细胞内活性氧和蛋白质印迹分析分析了相关机制。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 还显着降低了高糖诱导的炎症细胞因子，如 TNF-α、IL-1β 和 IL-6 的分泌，这也与 BDB 调节的 p65 蛋白表达和 NF-ĸB 活性的降低一致。 . 与单独的高葡萄糖处理相比，BDB 还下调了 38 种蛋白质表达的活性氧 (ROS) 产生和磷酸化。此外，BDB保留了高糖条件下内皮细胞迁移和管形成的功能，