Effect of glucagon-like peptide-1 on hypoxia-reoxygenation induced injury in neonatal rat cardiomyocytes / 中华心血管病杂志
Chinese Journal of Cardiology
; (12): 72-75, 2010.
Article
in Zh
| WPRIM
| ID: wpr-341282
Responsible library:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of glucagon-like peptide-1 (GLP-1) on hypoxia-reoxygenation (H/R) induced injury in neonatal rat cardiomyocytes.</p><p><b>METHODS</b>Cultured neonatal rat cardiomyocytes were randomly divided into seven groups normal control group, H/R group, GLP-1 + H/R group, GLP-1 + H/R + UO126 group, GLP-1 + H/R + LY294002 group, H/R + UO126 group, H/R + LY294002 group. LDH activity, apoptosis rate of cardiomyocytes, Caspase-3 activity were detected.</p><p><b>RESULTS</b>Compared with normal control group, the activity of LDH, cardiomyocyte apoptosis rate, Caspase-3 activity were all significantly increased in H/R group (all P < 0.01). However, compared with H/R group, these changes were significantly attenuated in GLP-1 + H/R group [the activity of LDH (128.47 +/- 7.96) U/L vs. (223.96 +/- 22.10) U/L, P < 0.01, and cardiomyocyte apoptosis rate (2.84 +/- 2.56)% vs. (12.58 +/- 6.69)%, P < 0.01, and Caspase-3 activity (36,809 +/- 4750) RLU vs. (57,602 +/- 9161) RLU, P < 0.01], while LY294002 (PI3K inhibitor) and UO126 (MAPK inhibitor) could block the effects of GLP-1 in cardiomyocytes underwent H/R injury.</p><p><b>CONCLUSIONS</b>GLP-1 could protect H/R injury mainly by inhibiting cardiomyocytes apoptosis via activating PI3K/Akt and MAPK signaling pathway.</p>
Full text:
1
Index:
WPRIM
Main subject:
Pharmacology
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Glucagon
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Myocardial Reperfusion Injury
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Cell Hypoxia
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Cells, Cultured
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Rats, Wistar
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Apoptosis
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Myocytes, Cardiac
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Glucagon-Like Peptide 1
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Caspase 3
Limits:
Animals
Language:
Zh
Journal:
Chinese Journal of Cardiology
Year:
2010
Type:
Article