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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Ischemia-reperfusion-induced changes in sarcolemmal Na+/K+-ATPase are due to the activation of calpain in the heart.
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Ischemia-reperfusion-induced changes in sarcolemmal Na+/K+-ATPase are due to the activation of calpain in the heart.

机译：缺血再灌注诱导的肌膜Na + / K + -ATPase改变是由于心脏中钙蛋白酶的激活所致。

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摘要

Depression in cardiac performance due to ischemia-reperfusion (I/R) injury is associated with the development of oxidative stress and decreased sarcolemmal (SL) Na+/K+-ATPase activity. Since both I/R and oxidative stress have been reported to promote the occurrence of intracellular Ca2+ overload and activate proteases such as calpain, this study was undertaken to investigate whether the activation of calpain in I/R hearts is associated with alterations in the SL Na+/K+-ATPase activity and its isoform content. For this purpose, isolated rat hearts treated with and without 2 different calpain inhibitors (leupeptin and MDL28170) were subjected to 30 min ischemia followed by 60 min of reperfusion, and the cardiac function, SL Na+/K+-ATPase activity, Na+/K+-ATPase isoform protein content, and calpain activity were measured. The I/R-induced depressions in cardiac function, Na+/K+-ATPase activity, and protein content of Na+/K+-ATPase isoforms were associated with an increase in calpain activity , but were prevented by treatment of hearts with leupeptin. Incubation of SL membranes with calpain decreased the Na+/K+-ATPase activity and protein content of its isoforms; these changes were also attenuated by leupeptin. The I/R-induced alterations in cardiac function and the activity of SL Na+/K+-ATPase and calpain were Ca2+-dependent and were prevented by MDL28170, a specific inhibitor of calpain. The I/R-induced translocation of calpain isoforms (I and II) from the cytosol to SL and the changes in distribution of calpastatin were also attenuated by treatment with calpain inhibitors. These results suggest that the depression in cardiac function and SL Na+/K+-ATPase activity in I/R hearts may be due to changes in the activity and translocation of calpain.
机译：缺血再灌注（I / R）损伤导致的心脏功能下降与氧化应激的发展和肌膜（SL）Na + / K + -ATPase活性降低有关。由于据报道I / R和氧化应激均会促进细胞内Ca2 +超负荷的发生并激活蛋白酶（例如钙蛋白酶），因此本研究旨在研究I / R心脏中钙蛋白酶的激活是否与SL Na +的改变有关/ K + -ATPase活性及其同工型含量。为此，对接受和不接受两种不同钙蛋白酶抑制剂（leupeptin和MDL28170）治疗的离体大鼠心脏进行30分钟缺血，然后再灌注60分钟，并测量其心脏功能，SL Na + / K + -ATPase活性，Na + / K +-测量了ATPase同工型蛋白含量和钙蛋白酶活性。 I / R诱导的心脏功能，Na + / K + -ATPase活性降低和Na + / K + -ATPase异构体的蛋白质含量与钙蛋白酶活性增加有关，但通过用亮肽素治疗心脏可以预防。将钙蛋白酶与SL膜一起孵育会降低Na + / K + -ATPase活性和亚型的蛋白质含量。这些变化也被亮肽素减弱。 I / R诱导的心脏功能改变以及SL Na + / K + -ATPase和钙蛋白酶的活性是Ca2 +依赖性的，可以被钙蛋白酶的特异性抑制剂MDL28170阻止。 I / R诱导的钙蛋白酶同工型（I和II）从胞质到SL的转运以及钙蛋白酶抑素分布的变化也通过钙蛋白酶抑制剂的治疗而减弱。这些结果表明I / R心脏的心脏功能下降和SL Na + / K + -ATPase活性降低可能是由于钙蛋白酶的活性和易位性改变所致。

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