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目的:探索姜黄素对高糖介导的血管氧化应激水平的升高和血管功能的保护作用未知及相关的机制。方法:以高糖DMEM培养基复制人脐静脉内皮细胞(HUVECs)的高糖损害模型。姜黄素干预24h后以DHE荧光探针分析姜黄素对高糖介导的活性氧产生的影响;分离健康C57BL/6J小鼠胸主动脉,以高糖DMEM培养基进行体外培养制作高糖介导的血管损害模型,分析姜黄素对高糖介导的血管功能的影响。利用western blotting方法检测血管内皮细胞中p-e NOS及p-AMPK的表达水平。结果:姜黄素可显著减少高糖介导的血管内皮细胞活性氧水平,该作用在给予AMPK抑制剂后显著降低;姜黄素可显著促进高糖环境血管内皮细胞e NOS的磷酸化并可显著改善高糖环境下小鼠胸主动脉的血管内皮依赖性舒张功能。Western blotting结果表明,姜黄素可显著增加p-AMPK的表达。结论:姜黄素显著减轻高糖血管内皮细胞的氧化应激水平,改善血管内皮依赖性舒张功能,而该作用可能与其通过激活AMPK/e NOS通路有关。
OBJECTIVE: To explore the unknown and related mechanism of curcumin on high glucose-induced increase of vascular oxidative stress and protection of vascular function. Methods: The hyperglycemic model of human umbilical vein endothelial cells (HUVECs) was induced by high glucose DMEM. Curcumin intervention 24h after DHE fluorescence probe analysis of high glucose-induced reactive oxygen species production; C57BL / 6J mice isolated thoracic aorta, with high glucose DMEM medium for in vitro production of high glucose mediated Of vascular damage model, analysis of curcumin on high glucose-mediated vascular function. Western blotting was used to detect the expression of p-e NOS and p-AMPK in vascular endothelial cells. Results: Curcumin significantly decreased the level of reactive oxygen species (ROS) in vascular endothelial cells induced by high glucose, which was significantly decreased after administration of AMPK inhibitor. Curcumin significantly enhanced eNOS phosphorylation in vascular endothelial cells Vascular Endothelium - Dependent Dilation Function of Thoracic Aorta in Mouse Under High Glucose Condition. Western blotting results showed that curcumin significantly increased p-AMPK expression. CONCLUSION: Curcumin significantly attenuates oxidative stress and improves endothelium-dependent vasodilatation in hyperglycemic vascular endothelial cells, which may be related to its activation of AMPK / e NOS pathway.