Pituitary adenylate cyclase activating polypeptide protects cardiomyocytes against oxidative stress-induced apoptosis

被引：67

作者：

Gasz, B

Rácz, B

Roth, E

Borsiczky, B

Ferencz, A

Tamás, A

Cserepes, B

Lubics, A

Gallyas, F

Tóth, G

Lengvári, I

Reglodi, D

机构：

[1] Univ Pecs, Fac Med, Dept Anat, Hungarian Acad Sci,Neurohumoral Regulat Res Grp, H-7624 Pecs, Hungary

[2] Univ Pecs, Fac Med, Dept Surg Res & Tech, Pecs, Hungary

[3] Univ Pecs, Fac Med, Dept Med Chem & Biochem, Pecs, Hungary

[4] Univ Szeged, Dept Med Chem, Szeged, Hungary

来源：

PEPTIDES | 2006年 / 27卷 / 01期

基金：

匈牙利科学研究基金会;

关键词：

cardiomyocyte; apoptosis; PACAP; cardioprotection;

D O I：

10.1016/j.peptides.2005.06.022

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Pituitary adenylate cyclase activating polypeptide (PACAP) has well-known neuroprotective effects, and one of the main factors leading to neuroprotection seems to be its anti-apoptotic effects. The peptide and its receptors are present also in the heart, but whether PACAP can be protective in cardiomyocytes, is not known. Therefore, the aim of the present study was to investigate the effects of PACAP on oxidative stress-induced apoptosis in cardiomyocytes. Our results show that PACAP increased cell viability by attenuating H2O2-induced apoptosis in a cardiac myocyte culture. PACAP also decreased caspase-3 activity and increased the expression of the anti-apoptotic markers Bcl-2 and phospho-Bad. These effects of PACAP were counteracted by the PACAP antagonist PACAP6-38. In summary, our results show that PACAP is able to attenuate oxidative stress-induced cardiomyocyte apoptosis. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：87 / 94

页数：8

共 64 条

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