垂体腺苷酸环化酶激活多肽可保护心肌细胞免受氧化应激诱导的凋亡。
Pituitary adenylate cyclase activating polypeptide protects cardiomyocytes against oxidative stress-induced apoptosis.
作者信息
Gasz B, Rácz B, Roth E, Borsiczky B, Ferencz A, Tamás A, Cserepes B, Lubics A, Gallyas F, Tóth G, Lengvári I, Reglodi D
机构信息
Department of Surgical Research and Techniques, Medical Faculty, Pécs University, Hungary.
出版信息
Peptides. 2006 Jan;27(1):87-94. doi: 10.1016/j.peptides.2005.06.022. Epub 2005 Aug 10.
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.
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，而导致神经保护的主要因素之一似乎是其抗凋亡作用。该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，本研究的目的是探讨PACAP对氧化应激诱导的心肌细胞凋亡的影响。我们的结果表明，PACAP通过减轻H2O2诱导的心肌细胞培养物中的细胞凋亡来提高细胞活力。PACAP还降低了半胱天冬酶-3的活性，并增加了抗凋亡标志物Bcl-2和磷酸化Bad的表达。PACAP拮抗剂PACAP6-38可抵消PACAP的这些作用。总之，我们的结果表明，PACAP能够减轻氧化应激诱导的心肌细胞凋亡。
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