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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Exercise preconditioning provides early cardioprotection against exhaustive exercise in rats: Potential involvement of protein kinase C delta translocation
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Exercise preconditioning provides early cardioprotection against exhaustive exercise in rats: Potential involvement of protein kinase C delta translocation

机译:运动预处理可对大鼠进行力竭运动的早期心脏保护:蛋白激酶Cδ易位的潜在参与

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The objective of this study was to investigate the early cardioprotective effect of exercise preconditioning (EP) on the exhaustive exercise-induced myocardial injury in rats and the role of protein kinase C delta isoform (PKCd) in EP. Rats were subjected to run on the treadmill for four periods of 10 min each at 30 m/min with intervening periods of rest of 10 min as an EP protocol. The exhaustive exercise was performed 0.5 h after EP. PKC inhibitor chelerythrine (CHE) was injected before EP. Our results showed that EP markedly attenuated the exhaustive exercise-induced myocardial ischemia/hypoxia, ultrastructural damage, high serum c Tn I, and NT-pro BNP levels. CHE injection before EP did not abolish the protection of EP. Both exhaustive exercise and EP produced a significant increase in PKCσ and p-PKCσ Thr507 protein levels in cardiomyocytes. However, the immunostaining of p-PKCσ Thr507 in EP cardiomyocytes was primarily localized to intercalated disks and nuclei while the exhaustive exercise-induced high level p-PKCσ Thr507 was mainly distributed in the cytoplasm. Moreover, the high PKCσ and p-PKCσ Thr507 levels in exhaustive exercise were significantly down-regulated by EP. CHE did not attenuate the expressions of PKCσ and p-PKCσ Thr507. These results indicate that an appropriate activation and translocation of PKCd may represent a mechanism whereby EP can exert an early cardioprotection against exhaustive exerciseinduced myocardial injury.
机译:这项研究的目的是研究运动预处理(EP)对力竭运动诱发的大鼠心肌损伤的早期心脏保护作用,以及蛋白激酶Cδ亚型(PKCd)在EP中的作用。根据EP规程,大鼠在跑步机上以30 m / min的速度运行四个周期,每个周期为10分钟,其余10分钟为间隔。 EP后0.5小时进行彻底运动。在EP之前注射PKC抑制剂白屈菜红碱(CHE)。我们的研究结果表明,EP可以显着减轻运动引起的心肌缺血/缺氧,超微结构损害,血清c Tn I和NT-pro BNP水平升高。 EP之前的CHE注射并没有取消对EP的保护。力竭运动和EP均使心肌细胞的PKCσ和p-PKCσThr507蛋白水平显着增加。然而,EP心肌细胞中p-PKCσThr507的免疫染色主要定位于插层盘和细胞核,而力竭性运动诱导的高水平p-PKCσThr507主要分布在细胞质中。而且,极力运动中的高PKCσ和p-PKCσThr507水平被EP显着下调。 CHE不会减弱PKCσ和p-PKCσThr507的表达。这些结果表明,PKCd的适当激活和易位可能代表了一种机制,EP可以发挥早期心脏保护作用,以抵抗力竭运动引起的心肌损伤。

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