Involvement of p38 MAPK pathway in GLP-1-induced inhibition of apoptosis in human umbilical vein endothelial cells / 生理学报
Acta Physiologica Sinica
; (6): 444-448, 2012.
Article
in Zh
| WPRIM
| ID: wpr-333181
Responsible library:
WPRO
ABSTRACT
The aim of the present study was to investigate the effect of glucagon-like peptide-1 (GLP-1) on palmitate-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and the underlying mechanism. HUVECs were cultured in vitro, and then treated by palmitate to induce apoptosis. Meanwhile, GLP-1 was added to explore its effect. After 24 h of the treatments, Caspase-3 activity and DNA fragmentation were measured using ELISA kits. Phospho-p38 mitogen-activated protein kinase (p-p38 MAPK) expression was detected by Western blot. The results showed that incubating HUVECs with 0.125 mmol/L GLP-1 increased Caspase-3 activity and DNA fragmentation. GLP-1 significantly inhibited palmitate-induced increases of Caspase-3 activity and DNA fragmentation in a concentration-dependent manner. Moreover, GLP-1 inhibited the up-regulation of p-p38 MAPK expression induced by palmitate in HUVECs. These results suggest GLP-1 protects HUVECs against lipo-apoptosis, and this effect may be mediated through inhibiting p38 MAPK pathway.
Full text:
1
Database:
WPRIM
Main subject:
Up-Regulation
/
Apoptosis
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MAP Kinase Signaling System
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Cell Biology
/
P38 Mitogen-Activated Protein Kinases
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Glucagon-Like Peptide 1
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Caspase 3
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DNA Fragmentation
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Human Umbilical Vein Endothelial Cells
/
Metabolism
Limits:
Humans
Language:
Zh
Journal:
Acta Physiologica Sinica
Year:
2012
Document type:
Article