Objective     To explore the expression of fractalkine (FKN) and the apoptosis of human umbilical vein endothelial cells (HUVECs) induced by high glucose and its possible relationship with Wnt signaling pathway.     Methods     HUVECs in good condition were divided into 4 groups

normal group (DMEM+5.5 mmol/L glucose)

hig

h glucose group (HG

33.3 mmol/L glucose)

lithium chloride group (10 mmol/L LiCl)

and high glucose with lithium chloride group (HG+LiCl). After planted HUVECs in DMEM/LG (5.5 mmol/L) for 10 h

10 mmol/L LiCl was added for 2 h as above and then 33.3 mmol/L glucose was added for 48 h. The apoptosis of HUVECs were evaluated by TUNEL assay. Protein levels of intracellular β-catenin and p-GSK-3β (Ser

9

) were measured by immunohistochemistry staining (SABC). Expression of fractalkine was detected by immunofluorescence staining (FITC)

and the mRNA expressions of GSK-3β and FKN were measured by RT-PCR.     Results    High glucose significantly induced a higher apoptotic rate in HUVECs than in normal control (P0.05)

but this increase of apoptotic rate was partly inhibited by LiCl (P0.05)

though the apoptosis of HG+LiCl still higher than normal control (P0.05). Compare with normal control

HG suppressed the protein expressions of β-catenin and p-GSK-3β (Ser

9

) (P0.05)

increased the mRNA levels of GSK-3β (P0.05) and enhanced the fracalkine expression at both protein and mRNA levels (P0.05). Compare with HG

the protein levels of β-catenin and p-GSK-3β (Ser

9

) were improved (P0.05)

and the mRNA levels of GSK-3β (P0.05) and both the protein and mRNA  levels of fractalkine were decreased in HG+ LiCl (P0.05).     Conclusion     High glucose induces apoptosis of HUVECs

which may be through inhibiting Wnt signaling pathway and fractalkine upregulation.