Advanced glycation end products (AGEs) induce inflammation and contribute to the pathogenesis of atherosclerosis. Although many studies have demonstrated the protective effects of carotenoids against atherosclerosis, the effects of carotenoids on AGE-induced inflammation have not been characterized. As such, we aimed to identify carotenoids that provided protection against AGE-elicited inflammation. AGE-stimulated RAW264 macrophages were first evaluated for NO generation. Among 17 carotenoids tested, only siphonaxanthin significantly suppressed it. Next, mRNA expression levels were measured in RAW264 macrophages and human umbilical vascular endothelial cells following siphonaxanthin and AGE treatment. Siphonaxanthin significantly suppressed AGE-induced mRNA expression of interleukin-6 and cellular adhesion molecules, which are known to be important for the pathogenesis of atherosclerosis. Siphonaxanthin also significantly suppressed endoplasmic reticulum (ER) stress marker genes. A reporter gene assay revealed that siphonaxanthin, as well as an ER stress inhibitor, significantly inhibited AGE-induced nuclear factor-κB (NF-κB) activation. Altogether, mitigation of ER stress and subsequent NF-κB activation is one of the molecular mechanisms by which siphonaxanthin suppressed AGE-elicited inflammation. Siphonaxanthin is a carotenoid commonly found in standard diets and is considered relatively safe for human consumption, and hence, dietary intake of siphonaxanthin or siphonaxanthin-containing green algae could be beneficial in lowering the risk of developing atherosclerosis.

中文翻译：

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虹吸黄质，一种来自绿藻的类胡萝卜素，抑制晚期糖基化终产物诱导的炎症反应。

晚期糖基化终产物（AGEs）会引起炎症，并导致动脉粥样硬化的发病机理。尽管许多研究证明了类胡萝卜素对动脉粥样硬化的保护作用，但类胡萝卜素对AGE诱导的炎症的作用尚未得到表征。因此，我们旨在鉴定可提供针对AGE引起的炎症的保护作用的类胡萝卜素。首先评估AGE刺激的RAW264巨噬细胞的NO生成。在测试的17种类胡萝卜素中，只有西黄嘌呤能显着抑制它。接下来，在虹吸黄质和AGE处理后，测量RAW264巨噬细胞和人脐带血管内皮细胞中的mRNA表达水平。虹吸黄质明显抑制AGE诱导的IL-6和细胞粘附分子的mRNA表达，已知对动脉粥样硬化的发病机制很重要。虹吸黄质也显着抑制内质网（ER）应激标记基因。一项记者基因检测表明，虹吸黄质以及一种ER应激抑制剂可显着抑制AGE诱导的核因子-κB（NF-κB）活化。总之，减轻内质网应激和随后的NF-κB激活是虹吸黄嘌呤抑制AGE引起的炎症的分子机制之一。虹吸黄质是一种常见于标准饮食中的类胡萝卜素，被认为对人类食用相对安全，因此，饮食中摄入虹吸黄质或含有虹吸黄质的绿藻可以降低患动脉粥样硬化的风险。虹吸黄质也显着抑制内质网（ER）应激标记基因。一项记者基因检测表明，虹吸黄质以及一种ER应激抑制剂可显着抑制AGE诱导的核因子-κB（NF-κB）活化。总之，减轻内质网应激和随后的NF-κB激活是虹吸黄嘌呤抑制AGE引起的炎症的分子机制之一。虹吸黄质是一种常见于标准饮食中的类胡萝卜素，被认为对人类食用相对安全，因此，饮食中摄入虹吸黄质或含有虹吸黄质的绿藻可以降低患动脉粥样硬化的风险。虹吸黄质也显着抑制内质网（ER）应激标记基因。一项记者基因检测表明，虹吸黄质以及一种ER应激抑制剂可显着抑制AGE诱导的核因子-κB（NF-κB）活化。总之，减轻内质网应激和随后的NF-κB激活是虹吸黄嘌呤抑制AGE引起的炎症的分子机制之一。虹吸黄质是标准饮食中常见的类胡萝卜素，被认为对人类食用相对安全，因此，饮食中摄入虹吸黄质或含有虹吸黄质的绿藻可以降低患动脉粥样硬化的风险。显着抑制AGE诱导的核因子-κB（NF-κB）活化。总之，减轻内质网应激和随后的NF-κB激活是虹吸黄嘌呤抑制AGE引起的炎症的分子机制之一。虹吸黄质是一种常见于标准饮食中的类胡萝卜素，被认为对人类食用相对安全，因此，饮食中摄入虹吸黄质或含有虹吸黄质的绿藻可以降低患动脉粥样硬化的风险。显着抑制AGE诱导的核因子-κB（NF-κB）活化。总之，减轻内质网应激和随后的NF-κB激活是虹吸黄嘌呤抑制AGE引起的炎症的分子机制之一。虹吸黄质是一种常见于标准饮食中的类胡萝卜素，被认为对人类食用相对安全，因此，饮食中摄入虹吸黄质或含有虹吸黄质的绿藻可以降低患动脉粥样硬化的风险。