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Apelin 通过激活过氧化氢酶预防氧化应激相关的心肌肥厚。

Activation of catalase by apelin prevents oxidative stress-linked cardiac hypertrophy.

机构信息

Institut National de la Santé et de la Recherche Médicale (INSERM), U858, Toulouse, France.

出版信息

FEBS Lett. 2010 Jun 3;584(11):2363-70. doi: 10.1016/j.febslet.2010.04.025. Epub 2010 Apr 14.

Abstract

Adipose tissue secretes a variety of bioactive factors, which can regulate cardiomyocyte hypertrophy via reactive oxygen species (ROS). In the present study we investigated whether apelin affects ROS-dependent cardiac hypertrophy. In cardiomyocytes apelin inhibited the hypertrophic response to 5-HT and oxidative stress induced by 5-HT- or H(2)O(2) in a dose-dependent manner. These effects were concomitant to the increase in mRNA expression and activity of catalase. Chronic treatment of mice with apelin attenuated pressure-overload-induced left ventricular hypertrophy. The prevention of hypertrophy by apelin was associated with increased myocardial catalase activity and decreased plasma lipid hydroperoxide, as an index of oxidative stress. These results show that apelin behaves as a catalase activator and prevents cardiac ROS-dependent hypertrophy.

摘要

脂肪组织分泌多种生物活性因子,可通过活性氧(ROS)调节心肌细胞肥大。本研究旨在探讨apelin 是否影响 ROS 依赖性心肌肥大。在心肌细胞中,apelin 呈剂量依赖性抑制 5-HT 诱导的和由 5-HT 或 H2O2 诱导的氧化应激引起的心肌细胞肥大反应。这些作用与过氧化氢酶 mRNA 表达和活性的增加同时发生。用 apelin 慢性处理小鼠可减轻压力超负荷引起的左心室肥厚。apelin 预防肥大与心肌过氧化氢酶活性增加和血浆脂质氢过氧化物减少有关,后者是氧化应激的一个指标。这些结果表明,apelin 作为过氧化氢酶激活剂发挥作用,可防止 ROS 依赖性心肌肥大。

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