垂体腺苷酸环化酶激活肽可抑制氧化应激诱导的培养心肌细胞中丝裂原活化蛋白激酶依赖性凋亡途径的激活。
PACAP inhibits oxidative stress-induced activation of MAP kinase-dependent apoptotic pathway in cultured cardiomyocytes.
作者信息
Gasz Balazs, Rácz Boglarka, Röth Erzsebet, Borsiczky Balazs, Tamás Andrea, Boronkai Arpad, Gallyas Ferenc, Tóth Gabor, Reglodi Dora
机构信息
Department of Anatomy, University of Pécs, 7624 Pécs, Szigeti u 12. Hungary.
出版信息
Ann N Y Acad Sci. 2006 Jul;1070:293-7. doi: 10.1196/annals.1317.029.
The present article investigated the effect of pituitary adenylate cyclase-activating polypeptide (PACAP) on oxidative stress-induced apoptosis in neonatal rat cardiomyocytes. Our results show that PACAP decreased the ratio of apoptotic cells following H2O2 treatment. PACAP also diminished the activity of apoptosis signal-regulating kinase. 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 and suggest that its cardioprotective effect is mediated through inhibition of the MAP kinase-dependent apoptotic pathway.
本文研究了垂体腺苷酸环化酶激活多肽（PACAP）对新生大鼠心肌细胞氧化应激诱导凋亡的影响。我们的结果表明，PACAP降低了H2O2处理后凋亡细胞的比例。PACAP还降低了凋亡信号调节激酶的活性。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，并提示其心脏保护作用是通过抑制丝裂原活化蛋白激酶（MAP激酶）依赖性凋亡途径介导的。
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