The single intravenous administration of methylene blue after traumatic brain injury diminishes neurological deficit, blood-brain barrier disruption and decrease in the expression of S100 protein in rats

被引:13
|
作者
Genrikhs, Elizaveta E. [1 ]
Stelmashook, Elena, V [1 ]
Voronkov, Dmitriy N. [1 ]
Novikova, Svetlana, V [1 ]
Alexandrova, Olga P. [1 ]
Fedorov, Artem, V [2 ]
Isaev, Nickolay K. [1 ,2 ]
机构
[1] Res Ctr Neurol, Volokolamskoe Shosse 80, Moscow 125367, Russia
[2] Moscow MV Lomonosov State Univ, Biol Fac, Leninskiye Gory 1,B 12, Moscow 119234, Russia
基金
俄罗斯科学基金会;
关键词
Traumatic brain injury; Neuroprotection; Methylene blue; Blood-brain barrier; NEURONAL CELL-DEATH; NITRIC-OXIDE; NEUROPROTECTION; MITOCHONDRIA; ACTIVATION; RESPONSES; TOXICITY;
D O I
10.1016/j.brainres.2020.146854
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The protective effect of methylene blue (MB) was investigated on the model of focal one-sided traumatic brain injury (TBI) of the sensorimotor cortex region from 1 to 7 days after the injury. TBI caused a reliable disruption of the functions of the limbs contralateral to injury focus, an increase in the expression of 5100 protein and blood-brain barrier (BBB) permeability in the ipsilateral hemisphere. The single intravenous injection of MB (1 mg/kg body weight) 30 min after TBI significantly reduced the limb function impairment as well as a TBIinduced increase in the expression of inflammatory marker 5100 protein, and BBB permeability. When modeling inflammation in vitro, MB was found to protect cultured neurons from the toxic effects of lipopolysaccharide. In conclusion, the preservation of blood-brain barrier and a decrease in the expression of S100 protein may be an important mechanism by means of which MB improves neurological outcome. Our data demonstrate that MB can be a very promising pharmacological compound with neuroprotective properties for TBI treatment.
引用
收藏
页数:7
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