Effects of vinpocetine on cognitive function and the expression of Nogo -A in Hippocampus of chronic cerebral ischemia rats
10.13699/j.cnki.1001-6821.2015.24.022
- VernacularTitle:长春西汀对慢性脑缺血大鼠认知功能及海马区Nogo－A表达的影响
- Author:
Mei-Yue LONG
1
;
Guang HAO
;
Xiu-Zhen ZHAI
;
Zhi-Min LU
Author Information
1. 河北北方学院研究生院
- Keywords:
chronic cerebral ischemia;
cognitive function;
vinpocetine;
Nogo-A express
- From:
The Chinese Journal of Clinical Pharmacology
2015;(24):2440-2443
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of vinpocetine on lear-ning and memory function and the expression of Nogo-A in the hippo-campus CA1 region of the rats with chronic cerebral ischemia.Methods The chronic cerebral ischemia rats model was induced by bilateral common carotid artery permanent occlusion. The rats were randomly divided into sham operation, model and experimental groups.Each group according to ischemic time was subdivided into 3 , 6 and 9 weeks groups. The rats in experimental group were injected vinpocetine intraperitoneally ( ip by 10 mg? kg -1 ) , once a day for consecutive 14 d.Cognitive func-tion of the rats were tested with the Morris water maze and the expression of Nogo -A was measured by immunohistochemistry and situ hibridiza-tion.Results After 6 weeks, the escape latency in the sham group, model group and the experimental group were ( 14.76 ± 4.34 ) , (33.23 ±3.42) , ( 27.74 ±5.30 ) s, respectively. The number of cross-platform were (6.88 ±2.64 ) , ( 3.13 ±1.81 ) , ( 5.38 ±1.85 ) times, respectively.Compared with model group, the average escape latency significantly shortened, the number that rats passed through the platform significantly increased ( P <0.05 ) , and the expression of Nogo-A protein and mRNA in hippocampal CA1 areas significantly increased ( P<0.05 ) in the experiment group at different time points. Conclusion Vinpocetine can improve the cognitive dysfunction of chronic cerebral ischemia rats which might be corre-lated to the neuroprotective effect of vinpocetine on neuronal by down-regulating the expressions of Nogo-A protein and mRNA.
