Abstract: Objective To investigate the role of p38MAPK signaling pathway in the mechanism by which glucagon-like
peptide-1 (GLP-1) inhibits endothelial cell damage induced by AGEs. Methods Human umbilical vein endothelial cells were
divided into control group, AGEs group, GLP-1 group, AGEs + GLP-1 group, AGEs + inhibitor group, and AGEs + GLP-1 +
inhibitor group. The expressions of p-p38MAPK/p38MAPK and p-eNOS/eNOS protein were examined by Western blotting,
and the cell apoptosis rates were tested by flow cytometry. Results Compared with the control group, AGEs significantly
enhanced the expression of p-p38 MAPK protein (P=0.001) while GLP-1 significantly inhibited its expression (P<0.001). AGEs
significantly inhibited the expression of p-eNOS protein (P=0.007), which was enhanced by GLP-1 and p38 MAPK inhibitor
(SB203580) (P=0.004). Both SB203580 and GLP-1 treatment decreased the apoptosis rate of AGEs-treated cells (P<0.001).
Conclusion GLP-1 can protect human umbilical vein endothelial cells against AGEs-induced apoptosis partially by inhibiting
the phosphorylation of p38MAPK protein and promoting the expression of p-eNOS protein.