期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 18, 页码 -出版社
MDPI
DOI: 10.3390/ijms231810921
关键词
ionizing radiation; skeletal muscle; Na; K-ATPase isozymes; ouabain; resting membrane potential
资金
- Russian Science Foundation [18-15-00043]
This study investigated the protective effect of ouabain on ionizing radiation-induced disturbances in skeletal muscle Na,K-ATPase function. Ouabain was found to prevent depolarization and loss of electrogenic contribution of the alpha 2 isozyme of Na,K-ATPase, accompanied by an increase in circulating ouabain concentration.
The damaging effect of ionizing radiation (IR) on skeletal muscle Na,K-ATPase is an open field of research. Considering a therapeutic potential of ouabain, a specific ligand of the Na,K-ATPase, we tested its ability to protect against the IR-induced disturbances of Na,K-ATPase function in rat diaphragm muscle that co-expresses the alpha 1 and alpha 2 isozymes of this protein. Male Wistar rats (n = 26) were subjected to 6-day injections of vehicle (0.9% NaCl) or ouabain (1 mu g/kg/day). On the fourth day of injections, rats were exposed to one-time total-body X-ray irradiation (10 Gy), or a sham irradiation. The isolated muscles were studied 72 h post-irradiation. IR decreased the electrogenic contribution of the alpha 2 Na,K-ATPase without affecting its protein content, thereby causing sarcolemma depolarization. IR increased serum concentrations of ouabain, IL-6, and corticosterone, decreased lipid peroxidation, and changed cellular redox status. Chronic ouabain administration prevented IR-induced depolarization and loss of the alpha 2 Na,K-ATPase electrogenic contribution without changing its protein content. This was accompanied with an elevation of ouabain concentration in circulation and with the lack of IR-induced suppression of lipid peroxidation. Given the crucial role of Na,K-ATPase in skeletal muscle performance, these findings may have therapeutic implications as countermeasures for IR-induced muscle pathology.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据