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Activation of Na + -K + -ATPase with DRm217 attenuates oxidative stress-induced myocardial cell injury via closing Na + -K + -ATPase/Src/Ros amplifier.

Reduced Na+ -K+ -ATPase activity has close relationship with cardiomyocyte death. Reactive oxygen species (ROS) also plays an important role in cardiac cell damage. It has been proved that Na+ -K+ -ATPase and ROS form a feed-forward amplifier. The aim of this study was to explore whether DRm217, a proved Na+ /K+ -ATPase's DR-region specific monoclonal antibody and direct activator, could disrupt Na+ -K+ -ATPase/ROS amplifier and protect cardiac cells from ROS-induced injury. We found that DRm217 protected myocardial cells against hydrogen peroxide (H2 O2 )-induced cardiac cell injury and mitochondrial dysfunction. DRm217 also alleviated the effect of H2 O2 on inhibition of Na+ -K+ -ATPase activity, Na+ -K+ -ATPase cell surface expression, and Src phosphorylation. H2 O2 -treatment increased intracellular ROS, mitochondrial ROS and induced intracellular Ca2+ , mitochondrial Ca2+ overload. DRm217 closed Na+ -K+ -ATPase/ROS amplifier, alleviated Ca2+ accumulation and finally inhibited ROS and mitochondrial ROS generation. These novel results may help us to understand the important role of the Na+ -K+ -ATPase in oxidative stress and oxidative stress-related disease.

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