中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
Chinese Journal of Pathophysiology
2015年
9期
1693-1698
,共6页
梓醇%氧化应激%炎症反应%晚期糖基化终产物受体
梓醇%氧化應激%炎癥反應%晚期糖基化終產物受體
재순%양화응격%염증반응%만기당기화종산물수체
Catalpol%Oxidative stress%Inflammation%Receptor for advanced glycation end products
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。
目的：研究梓醇對晚期糖基化終產物（ AGEs）誘導的EA．hy926內皮細胞炎癥反應的抑製作用併探討其可能機製。方法：將常規培養的EA．hy926細胞隨機分為對照組、梓醇對照組、AGEs 組以及梓醇高劑量（0．5 mmol／L）、中劑量（0．25 mmol／L）和低劑量（0．05 mmol／L）保護組。激光共聚焦顯微鏡觀察細胞內活性氧簇（ ROS）的生成；RT－PCR和Western blot檢測細胞中單覈細胞趨化蛋白1（ MCP－1）、腫瘤壞死因子α（ TNF－α）、血管細胞黏附分子1（VCAM－1）及晚期糖基化終產物受體（RAGE）的mRNA及蛋白的錶達。結果：梓醇保護組ROS生成均明顯減少，MCP－1、TNF－α和VCAM－1的mRNA及蛋白錶達均顯著降低，RAGE蛋白錶達明顯受抑製，且呈劑量依賴性（P＜0．05）。結論：梓醇能夠有效抑製AGEs誘導的EA．hy926細胞內氧化應激，減輕炎癥反應，其機製可能與其降低RAGE錶達有關。
목적：연구재순대만기당기화종산물（ AGEs）유도적EA．hy926내피세포염증반응적억제작용병탐토기가능궤제。방법：장상규배양적EA．hy926세포수궤분위대조조、재순대조조、AGEs 조이급재순고제량（0．5 mmol／L）、중제량（0．25 mmol／L）화저제량（0．05 mmol／L）보호조。격광공취초현미경관찰세포내활성양족（ ROS）적생성；RT－PCR화Western blot검측세포중단핵세포추화단백1（ MCP－1）、종류배사인자α（ TNF－α）、혈관세포점부분자1（VCAM－1）급만기당기화종산물수체（RAGE）적mRNA급단백적표체。결과：재순보호조ROS생성균명현감소，MCP－1、TNF－α화VCAM－1적mRNA급단백표체균현저강저，RAGE단백표체명현수억제，차정제량의뢰성（P＜0．05）。결론：재순능구유효억제AGEs유도적EA．hy926세포내양화응격，감경염증반응，기궤제가능여기강저RAGE표체유관。
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 .
