scholarly journals Fibroblast growth factor 2 contributes to the effect of salidroside on dendritic and synaptic plasticity after cerebral ischemia/reperfusion injury

Aging ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 10951-10968 ◽  
Author(s):  
Sisi Li ◽  
Yechen Lu ◽  
Daofang Ding ◽  
Zhenzhen Ma ◽  
Xiangxin Xing ◽  
...  
2020 ◽  
Vol 14 ◽  
Author(s):  
Wenzhu Wang ◽  
Xu Liu ◽  
Zhengyi Yang ◽  
Hui Shen ◽  
Lixu Liu ◽  
...  

The cognitive impairment caused by cerebral ischemia/reperfusion is an unsolved problem in the field of international neural rehabilitation. Not only ameliorates the consciousness level of certain patients who suffered from ischemia-reperfusion injury and were comatose for a long time period after cerebral resuscitation treatment, but levodopa also improves the symptoms of neurological deficits in rats with global cerebral ischemia-reperfusion injury. However, Levodopa has not been widely used as a brain protection drug after cardiopulmonary resuscitation, because of its unclear repair mechanism. Levodopa was used to study the neuroplasticity in the hippocampus of global cerebral ischemia/reperfusion injury rat model, established by Pulsinelli's four-vessel occlusion method. Levodopa was injected intraperitoneally at 50 mg/kg/d for 7 consecutive days after 1st day of surgery. The modified neurological function score, Morris water maze, magnetic resonance imaging, Nissl and TH staining, electron microscopy and western blot were used in the present study. The results showed that levodopa improved the neurological function and learning and memory of rats after global cerebral ischemia/reperfusion injury, improved the integrity of white matter, and density of gray matter in the hippocampus, increased the number of synapses, reduced the delayed neuronal death, and increased the expression of synaptic plasticity-related proteins (BDNF, TrkB, PSD95, and Drebrin) in the hippocampus. In conclusion, levodopa can improve cognitive function after global cerebral ischemia/reperfusion injury by enhancing the synaptic plasticity in the hippocampus.


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