中文摘要：

目的探讨二氢杨梅素对高糖诱导血管内皮细胞凋亡的影响及其与磷酸腺苷活化蛋白激酶（AMP-activated protein kinase,AMPK）的关系。方法体外培养原代人脐带静脉内皮细胞（human umbilical vein endothelial cells,HUVECs）,分为正常对照组（5.56 mmol/L葡萄糖）、高糖处理组（33.36 mmol/L葡萄糖）、甘露醇高渗对照组（5.56 mmol/L葡萄糖＋27.8 mmol/L甘露醇）、AMPK激动剂5-氨基咪唑-4-甲酰胺-1-β-D-呋喃核糖苷（5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranoside,AICAR）（10 nmol/L）＋高糖处理组、二氢杨梅素（1μmol/L）＋高糖处理组、AMPK抑制剂compound C（5 mmol/L）＋AICAR＋高糖处理组和AMPK抑制剂compound C（5 mmol/L）＋二氢杨梅素＋高糖处理组。处理36 h后,CCK-8法检测细胞增殖活力,Annexin V-FITC/PI双标记流式细胞仪检测细胞凋亡,Western blot法检测AMPK、p-AMPK、乙酰辅酶A羧化酶（Acetyl-Co A carboxylase,ACC）和p-ACC蛋白水平。结果与正常对照组比较,高糖处理组细胞活力明显降低（P〈0.05）,细胞凋亡率显著增加（P〈0.05）,p-AMPK、p-ACC水平显著降低（P〈0.05）;二氢杨梅素或AICAR预处理均明显抑制高糖诱导的HUVECs细胞活力下降、细胞凋亡增加和p-AMPK、p-ACC水平降低（P〈0.05）;Compound C预处理明显抑制AICAR和二氢杨梅素对高糖诱导HUVECs细胞凋亡的保护作用（P〈0.05）。结论二氢杨梅素通过促进AMPK活化抑制高糖诱导的血管内皮细胞凋亡。

英文摘要：

Objective To determine the effects of dihydromyricetin（ DHM） on high glucose-induced apoptosis of vascular endothelial cells and its association with AMP-activated protein kinase（ AMPK）.Methods Human umbilical vascular endothelial cells（ HUVECs） were cultured in vitro,and then divided into normal control（ 5. 56 mmol / L glucose）,high glucose group（ 33. 36 mmol / L glucose）,osmotic control group（ 5. 56 mmol / L glucose and 27. 8 mmol / L mannitol）, 5-Aminoimidazole-4-carboxamide-1-β-Dribofuranoside（ AICAR） combined with high glucose group（ 10 nmol / L AMPK activator AICAR）,DHM combined with high glucose group（ 1 μmol / L dihydromyricetin）,compound C combined with AICAR and high glucose group（ 5 mmol / L AMPK inhibitor compound C）,and compound C combined with DHM and high glucose group. After 36 h cultivation,cell viability and apoptosis were detected by CCK-8 assay and Annexin V-FITC / PI double staining using flow cytometry,respectively. Western blotting was used to detect the expression levels of intracellular proteins AMPK,p-AMPK,Acetyl-Co A carboxylase（ ACC）,and p-ACC.Results Compared with the normal control group,high glucose significantly decreased cell viability（ P 〈0. 05）,increased the apoptotic rate（ P 〈 0. 05）,and decreased the expression levels of p-AMPK and p-ACC（ P 〈 0. 05）. The pretreatment of DHM or AICAR significantly inhibited these alterations induced by high glucose. However,the pretreatment of compound C significantly inhibited the protective effects of DHM and AICAR on high glucose-induced apoptosis in vascular endothelial cells（ P 〈 0. 05）. Conclusion DHM inhibits high glocose-induced HUVECs apoptosis through promoting the activation of AMPK.