Na+, K+-ATPase participates in the protective mechanism of rat cerebral ischemia-reperfusion through the interaction with glutamate transporter-1

被引：9

作者：

Li, Lin-Lin ^{[1
]}

Ke, Xue-Ying ^{[1
]}

Jiang, Chen ^{[2
]}

Qin, Shi-Qi ^{[1
]}

Liu, Yang-Yang ^{[1
]}

Xian, Xiao-Hui ^{[3
]}

Liu, Li-Zhe ^{[3
]}

He, Jin-Chen ^{[1
]}

Chen, Ya-Meng ^{[1
]}

An, Hong-Fei ^{[1
]}

Sun, Nan ^{[1
]}

Hu, Yue-Hua ^{[1
]}

Zhang, Li-Nan ^{[3
]}

Wang, Yan ^{[4
]}

Lu, Qi-Yong ^{[5
]}

机构：

[1] Hebei Med Univ, Basic Med Coll, Shijiazhuang, Hebei, Peoples R China

[2] Hebei Med Univ, Forens Med Coll, Shijiazhuang, Hebei, Peoples R China

[3] Hebei Med Univ, Dept Pathophysiol, Shijiazhuang, Hebei, Peoples R China

[4] North China Univ Sci & Technol Affiliated Hosp, Shijiazhuang, Hebei, Peoples R China

[5] Hengshui Fifth Peoples Hosp, Dept Neurosurg, Hengshui, Hebei, Peoples R China

来源：

FUNDAMENTAL & CLINICAL PHARMACOLOGY | 2021年 / 35卷 / 05期

关键词：

cerebral ischemia‐ reperfusion; glutamate transporter‐ 1; middle cerebral artery occlusion; Na plus; K+‐ ATPase; α subunit; OXYGEN-GLUCOSE DEPRIVATION; BRAIN ISCHEMIA; RELEASE; ASTROCYTES; EXPRESSION; HIPPOCAMPUS; INVOLVEMENT; INHIBITION; DISRUPTION; RILUZOLE;

D O I：

10.1111/fcp.12652

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Glutamate excitotoxicity in cerebral ischemia/reperfusion is an important cause of neurological damage. The aim of this study was to investigate the mechanism of Na+, K+-ATPase (NKA) involved in l ow concentration of ouabain (Oua, activating NKA)-induced protection of rat cerebral ischemia-reperfusion injury. The 2,3,5-triphenyltetrazolium chloride (TTC) staining and neurological deficit scores (NDS) were performed to evaluate rat cerebral injury degree respectively at 2 h, 6 h, 1 d and 3 d after reperfusion of middle cerebral artery occlusion (MCAO) 2 h in rats. NKA alpha 1/alpha 2 subunits and glutamate transporter-1 (GLT-1) protein expression were investigated by Western blotting. The cerebral infarct volume ratio were evidently decreased in Oua group vs MCAO/R group at 1 d and 3 d after reperfusion of 2 h MCAO in rats (*p 0.05 ). Moreover, NDS were not significantly different (p0.05 ). NKA alpha 1 was decreased at 6 h and 1 d after reperfusion of 2 h MCAO in rats, and was improved in Oua group. However, NKA alpha 1 and alpha 2 were increased at 3 d after reperfusion of 2 h MCAO in rats, and was decreased in Oua group. GLT-1 was decreased at 6 h, 1 d and 3 d after reperfusion of 2 h MCAO in rats, and was improved in Oua group. These data indicated that l ow concentration of Oua could improve MCAO/R injury through probably changing NKA alpha 1/alpha 2 and GLT-1 protein expression, then increasing GLT-1 function and promoting Glu transport and absorption, which could be useful to determine potential therapeutic strategies for patients with stroke. Low concentration of Oua improved rat MCAO/R injury via NKA alpha 1/alpha 2 and GLT-1.

引用

页码：870 / 881

页数：12

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