Alginate oligosaccharide (AOS) was reported to possess antioxidant and free radical scavenging activities, but the specific effects and mechanisms remain unclear. We investigated the effects of AOS on H2O2-induced oxidative stress and apoptosis in human umbilical vein endothelial cells (HUVECs) and the associated mechanisms. HUVECs were treated with 100-800 µM hydrogen peroxide (H2O2) for various periods (12, 24, and 36 h) to establish an in vitro oxidative stress and apoptosis HUVEC model. AOS protects HUVEC cells against oxidative stress-induced apoptosis by decreasing the expression levels of caspase 3 and Bax, and increasing Bcl-2 expression. Microarray assay, real-time PCR and western blot results revealed that AOS was able to effectively suppress H2O2-induced apoptosis via regulated integrin-α/FAK/PI3K pathway by influencing the expression of integrin-α, FAK, PI3K, PTEN, P21, and CDK2. In conclusion, our study suggests that AOS can protect endothelial cells against oxidative stress injury caused by H2O2, providing novel alternative strategies to prevent atherosclerosis in the future.

中文翻译：

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海藻寡糖通过整合素-α/FAK/PI3K 信号保护内皮细胞免受氧化应激损伤

据报道，海藻寡糖（AOS）具有抗氧化和清除自由基的活性，但其具体作用和机制尚不清楚。我们研究了 AOS 对 H2O2 诱导的人脐静脉内皮细胞 (HUVEC) 氧化应激和细胞凋亡的影响以及相关机制。HUVEC 用 100-800 µM 过氧化氢 (H2O2) 处理不同时间段（12、24 和 36 小时），以建立体外氧化应激和凋亡 HUVEC 模型。AOS 通过降低 caspase 3 和 Bax 的表达水平以及增加 Bcl-2 的表达来保护 HUVEC 细胞免受氧化应激诱导的细胞凋亡。微阵列分析，实时荧光定量 PCR 和蛋白质印迹结果表明，AOS 能够通过调节 integrin-α/FAK/PI3K 通路通过影响 integrin-α、FAK、PI3K、PTEN、P21 和 CDK2 的表达来有效抑制 H2O2 诱导的细胞凋亡。总之，我们的研究表明，AOS 可以保护内皮细胞免受 H2O2 引起的氧化应激损伤，为未来预防动脉粥样硬化提供新的替代策略。