Ecklonia cava extracts inhibit lipopolysaccharide induced inflammatory responses in human endothelial cells
Ecklonia cava extracts inhibit lipopolysaccharide induced inflammatory responses in human endothelial cells
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DOI：
10.1016/j.fct.2010.03.045
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发表时间：
2010-06-01
影响因子：
4.3
通讯作者：
Bae, Jong-Sup
中科院分区：
文献类型：
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作者：
Kim, Tae Hoon;Bae, Jong-Sup
Ecklonia cava (EC) 是一种褐藻，具有自由基清除、杀菌、酪氨酸酶抑制和蛋白酶抑制活性。然而，人们对人内皮细胞的抗炎作用及其分子机制仍知之甚少。在本研究中，我们试图确定 EC 提取物预处理是否能显着抑制脂多糖 (LPS) 诱导的人内皮细胞的抗炎活性。我们发现每种 EC 提取物都能抑制 LPS 诱导的屏障通透性、细胞粘附分子的表达、单核细胞粘附以及跨内皮迁移至人内皮细胞。进一步的研究表明，EC 提取物可抑制肿瘤坏死因子-α (TNF-α) 的产生和核因子-κ B (NF-κ B) 的激活。特别是，乙酸乙酯（EtOAc）和丁醇（n-BuOH）提取物的抗炎作用优于其他提取物。总的来说，这些结果表明，EC 提取物通过阻断 NF-κ B 表达的激活和 TNF-α 的产生，具有屏障完整性活性、对细胞粘附和迁移至内皮细胞的抑制活性，从而证实了其作为血管炎症疾病治疗的有用性。 (C) 2010 Elsevier Ltd. 保留所有权利。
Ecklonia cava (EC) is a brown alga that evidences radical scavenging, bactericidal, tyrosinase inhibitory and protease inhibitory activities. However, the antiinflammatory effects in human endothelial cells and its molecular mechanism remain poorly understood. In this study, we attempted to determine whether pretreatment with EC extracts induce a significant inhibition of antiinflammatory activities in lipopolysaccharide (LPS) induced human endothelial cells. We found that each EC extract inhibits LPS induced barrier permeability, expression of cell adhesion molecules, monocytes adhesion, and transendothelial migration to human endothelial cells. Further studies revealed that EC extracts suppress the production of tumor necrosis factor-alpha (TNF-alpha) and activation of nuclear factor-kappa B (NF-kappa B). Particularly, the antiinflammatory effects of ethyl acetate (EtOAc) and butanol (n-BuOH) extracts were better than those of other extracts. Collectively, these results suggest that EC extracts possess barrier integrity activity, inhibitory activity on cell adhesion and migration to endothelial cells by blocking the activation of NF-kappa B expression and production of TNF-alpha, thereby endorsing its usefulness as therapy for vascular inflammatory diseases. (C) 2010 Elsevier Ltd. All rights reserved.