与活性氧形成相关的过程不一定涉及异丙肾上腺素诱导的心脏肥大的发展。斯托巴定的作用。

Biomedica biochimica acta Pub Date : 1991-01-01
O Ondrejicková, A Dzurba, J Sedlák, J Tokárová, T Macicková, L Benes
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引用次数: 0

摘要

施斯托巴定(一种正在研究的心脏保护物质)可防止高剂量异丙肾上腺素(ISO) (30mg /kg)处理的大鼠心脏中蛋白质SH组和谷胱甘肽含量的下降。此外,斯托巴定还降低了异源性动物心脏线粒体中丙二醛含量、过氧化氢酶和谷胱甘肽还原酶活性的升高,以及GSH/GSSG比值的降低。由于斯托巴定可以被认为是一种活性氧(ROS)的清除剂,后一种物质的上述作用支持了活性氧(ROS)可能参与由剂量的ISO引起的心脏肥厚的某些过程的假设。然而,我们的研究结果也表明,ros介导的过程不一定参与诱导心肌肥厚本身的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Processes linked to the formation of reactive oxygen species are not necessarily involved in the development of isoproterenol-induced hypertrophy of the heart. The effect of stobadine.

Administration of stobadine, a cardioprotective substance in investigation prevents a decrease in the content of protein SH groups and glutathione in hearts of rats treated with high doses of isoproterenol (ISO) (30 mg/kg). Moreover, stobadine also attenuated the increase in the content of malondialdehyde and activities of catalase and glutathione reductase as well as a diminution in the GSH/GSSG ratio observed in heart mitochondria isolated from ISO-treated animals. Since stobadine may be considered as a scavenger of reactive oxygen species (ROS), the above effects of the latter substance support the assumption about a possible involvement of reactive oxygen species (ROS) in some processes initiated by administration of ISO in doses inducing cardiac hypertrophy. However our results also indicate that ROS-mediated processes are not necessarily involved in the mechanism of induction of cardiac hypertrophy itself.

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