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-D-ribofuranoside (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-CoA carboxylase (ACC)

and p-ACC.       Results       Compared with the normal control group

high glucose significantly decreased cell viability (P0.05)

increased the apoptotic rate (P0.05)

and decreased the expression levels of p-AMPK and p-ACC (P0.05). 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 (P0.05).       Conclusion       DHM inhibits high glocose-induced HUVECs apoptosis through promoting the activation of AMPK.