梓醇抑制 AGEs 诱导的 EA．hy926细胞炎症反应及 RAGE 表达

摘要

AIM:To investigate the inhibitory effect of catalpol on inflammation in EA .hy926 cells induced by advanced glycation end products ( AGEs) and to explore its antioxidant mechanisms .METHODS:Human endothelial cell line EA.hy926 was cultured and randomly divided into control group , catalpol (0.5 mmol/L) group, AGEs group, high-dose (0.5 mmol/L) catalpol +AGEs group, middle-dose (0.25 mmol/L) catalpol +AGEs group and low-dose (0.05 mmol/L) catalpol+AGEs group.Intracellular reative oxygen species ( ROS) production was detected by laser scanning confocal microscopy.The levels of monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-α(TNF-α) and vas-cular cell adhesion molecule-1 (VCAM-1) in culture supernatant were detected by commercial ELISA kits .The expression of MCP-1, TNF-α, VCAM-1 and receptor for advanced glycation end products (RAGE) in the EA.hy926 cells were detec-ted by Western blot.RESULTS:In high-dose catalpol+AGEs and middle-dose catalpol+AGEs groups, the generation of ROS was decreased significantly .The levels of MCP-1, TNF-αand VCAM-1, and protein expression of MCP-1, TNF-αand VCAM-1 were significantly lower .The expression of RAGE protein in EA .hy926 cells were significantly inhibited ( P<0.05).CONCLUSION:Catalpol effectively inhibits the AGEs-induced oxidative stress and inflammation in EA .hy926 cells, which may be associated with a decrease in the expression of RAGE .%目的：研究梓醇对晚期糖基化终产物（ AGEs）诱导的EA．hy926内皮细胞炎症反应的抑制作用并探讨其可能机制。方法：将常规培养的EA．hy926细胞随机分为对照组、梓醇对照组、AGEs 组以及梓醇高剂量（0．5 mmol／L）、中剂量（0．25 mmol／L）和低剂量（0．05 mmol／L）保护组。激光共聚焦显微镜观察细胞内活性氧簇（ ROS）的生成；RT－PCR和Western blot检测细胞中单核细胞趋化蛋白1（ MCP－1）、肿瘤坏死因子α（ TNF－α）、血管细胞黏附分子1（VCAM－1）及晚期糖基化终产物受体（RAGE）的mRNA及蛋白的表达。结果：梓醇保护组ROS生成均明显减少，MCP－1、TNF－α和VCAM－1的mRNA及蛋白表达均显著降低，RAGE蛋白表达明显受抑制，且呈剂量依赖性（P＜0．05）。结论：梓醇能够有效抑制AGEs诱导的EA．hy926细胞内氧化应激，减轻炎症反应，其机制可能与其降低RAGE表达有关。