Pituitary adenylate cyclase activating polypeptide protects cardiomyocytes against oxidative stress-induced apoptosis
Pituitary adenylate cyclase activating polypeptide protects cardiomyocytes against oxidative stress-induced apoptosis
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DOI：
10.1016/j.peptides.2005.06.022
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发表时间：
2006-01-01
期刊：
影响因子：
3
通讯作者：
Reglodi, D
中科院分区：
文献类型：
--
作者：
Gasz, B;Rácz, B;Reglodi, D
垂体腺苷酸环化酶激活多肽（垂体腺苷酸环化酶激活多肽，PACAP）具有众所周知的神经保护作用，其抗凋亡作用似乎是导致神经保护的主要因素之一。这种肽及其受体也存在于心脏中，但PACAP是否对心肌细胞具有保护作用尚不清楚。因此，本研究旨在探讨PACAP对氧化应激诱导的心肌细胞凋亡的影响。我们的研究结果表明，在心肌细胞培养中，PACAP通过减弱h2o2诱导的细胞凋亡来提高细胞活力。PACAP还降低了caspase-3活性，增加了抗凋亡标志物Bcl-2和phospho-Bad的表达。这些作用被PACAP拮抗剂PACAP6-38所抵消。总之，我们的研究结果表明，PACAP能够减轻氧化应激诱导的心肌细胞凋亡。(c) 2005爱思唯尔公司版权所有。
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.