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冬瓜对高糖诱导的人脐静脉内皮细胞血管炎症的影响。

Effect of Benincasa hispida Cogniaux on high glucose-induced vascular inflammation of human umbilical vein endothelial cells.

作者信息

Moon Mi Kyoung, Kang Dae Gill, Lee Yun Jung, Kim Jin Sook, Lee Ho Sub

机构信息

Professional Graduate School of Oriental Medicine Wonkwang University, Iksan, Jeonbuk, 570-749, Republic of Korea.

出版信息

Vascul Pharmacol. 2009 Mar-Apr;50(3-4):116-22. doi: 10.1016/j.vph.2008.11.007. Epub 2008 Nov 27.

Abstract

Vascular inflammation is an important factor which can promote diabetic complications. Preliminary investigations of several crude plant extracts including aqueous extract of Benincasa hispida Cogniaux exhibit anti-inflammatory properties. This study investigates the mechanism of anti-vascular inflammatory activity of an aqueous extract of B. hispida Cogniaux (ABH) in human umbilical vein endothelial cells (HUVECs). The study was performed on HUVECs that were pretreated with various concentrations (1-20 microg/ml) of ABH before exposure with high glucose (25 mM) for 48 h. Cell ELISA and Western blot analysis showed that ABH inhibited high glucose-induced cell adhesion molecules (CAMs) surface and protein expression, resulting in reduced adhesion of U937 monocytes. ABH also inhibited the mRNA expression level of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8). High glucose-induced ROS production was inhibited by treatment of ABH. We observed that pretreatment with HUVECs with ABH blocks NF-kappaB activation via blocking phosphorylation and degradation of its inhibitory protein, IkappaB-alpha. ABH also reduced NF-kB promoter activity. These results suggest that ABH reduces high glucose-induced CAMs activation by inhibiting monocyte adhesion, ROS, and NF-kappaB in HUVECs.

摘要

血管炎症是促进糖尿病并发症的一个重要因素。对包括冬瓜(Benincasa hispida Cogniaux)水提取物在内的几种植物粗提物的初步研究显示出抗炎特性。本研究调查了冬瓜水提取物(ABH)在人脐静脉内皮细胞(HUVECs)中抗血管炎症活性的机制。该研究在HUVECs上进行,这些细胞在暴露于高糖(25 mM)48小时之前,先用不同浓度(1 - 20微克/毫升)的ABH进行预处理。细胞酶联免疫吸附测定(Cell ELISA)和蛋白质印迹分析表明,ABH抑制了高糖诱导的细胞黏附分子(CAMs)的表面表达和蛋白质表达,从而减少了U937单核细胞的黏附。ABH还抑制了单核细胞趋化蛋白-1(MCP-1)和白细胞介素-8(IL-8)的mRNA表达水平。ABH处理抑制了高糖诱导的活性氧(ROS)产生。我们观察到,用ABH预处理HUVECs可通过阻断其抑制蛋白IkappaB-alpha的磷酸化和降解来阻断核因子-κB(NF-κB)的激活。ABH还降低了NF-κB启动子活性。这些结果表明,ABH通过抑制HUVECs中的单核细胞黏附、ROS和NF-κB来降低高糖诱导的CAMs激活。

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