...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Melatonin attenuates hypertension-related proarrhythmic myocardial maladaptation of connexin-43 and propensity of the heart to lethalarrhythmias
【24h】

Melatonin attenuates hypertension-related proarrhythmic myocardial maladaptation of connexin-43 and propensity of the heart to lethalarrhythmias

机译：褪黑素减轻与连接蛋白43相关的高血压相关的心律失常性心肌适应不良和心脏致死性心律失常的倾向

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We hypothesized that the pineal hormone melatonin, which exhibits cardioprotective effects, might affect myocardial expression of cell-to-cell electrical coupling protein connexin-43 (Cx43) and protein kinase C (PKC) signaling, and hence, the propensity of the heart to lethal ventricular fibrillation (VF). Spontaneously hypertensive (SHR) and normotensive Wistar rats fed a standard rat chow received melatonin (40 g/mL in drinking water during the night) for 5 weeks, and were compared with untreated rats. Melatonin significantly reduced blood pressure and normalized triglycerides in SHR, whereas it decreased body mass and adiposity in Wistar rats. Compared with healthy rats, the threshold to induce sustained VF was significantly lower in SHR (18.3 ± 2.6 compared with 29.2 ± 5 mA; p < 0.05) and increased in melatonin-treated SHR and Wistar rats to 33.0 ± 4 and 32.5 ± 4 mA. Melatonin attenuated abnormal myocardial Cx43 distribution in SHR, and upregulated Cx43 mRNA, total Cx43 protein, and its functional phosphorylated forms in SHR, and to a lesser extent, in Wistar rat hearts. Moreover, melatonin suppressed myocardial proapoptotic PKCδ expression and increased cardioprotective PKC3 expression in both SHR and Wistar rats. Our findings indicate that melatonin protects against lethal arrhythmias at least in part via upregulation of myocardial Cx43 and modulation of PKC-related cardioprotective signaling.
机译：我们假设具有心脏保护作用的松果激素褪黑激素可能会影响细胞间电连接蛋白connexin-43（Cx43）和蛋白激酶C（PKC）信号传导的心肌表达，因此会影响心脏致命性室颤（VF）。喂食标准大鼠食物的自发性高血压（SHR）和血压正常的Wistar大鼠接受褪黑素治疗（夜间在饮用水中浓度为40 g / mL），持续5周，并与未治疗的大鼠进行比较。褪黑激素可以显着降低SHR中的血压并使甘油三酯正常化，而它可以降低Wistar大鼠的体重和肥胖。与健康大鼠相比，SHR诱导持续VF的阈值明显降低（18.3±2.6与29.2±5 mA相比; p <0.05），而褪黑素治疗的SHR和Wistar大鼠则增加至33.0±4和32.5±4 mA 。褪黑素减弱了SHR中心肌Cx43的异常分布，并上调了Wistar大鼠心脏中Sx中Cx43 mRNA，总Cx43蛋白及其功能磷酸化形式的水平，但程度较小。此外，褪黑素在SHR和Wistar大鼠中均抑制了心肌细胞凋亡PKCδ的表达，并增加了心肌保护性PKC3的表达。我们的发现表明，褪黑激素至少部分通过心肌Cx43的上调和PKC相关的心脏保护信号的调节来预防致命性心律失常。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号