[Effect of salvianolic acid B on neural cells damage and neurogenesis after brain ischemia-reperfusion in rats].
Yao Xue Xue Bao
; 42(7): 716-21, 2007 Jul.
Article
en Zh
| MEDLINE
| ID: mdl-17882954
This study is to observe the effect of salvianolic acid B (Sal B) on neural cells damage and neurogenesis in sub-granular zone (SGZ) and sub-ventricular zone (SVZ) after brain ischemia-reperfusion (I/R) in rats. A modified middle cerebral artery occlusion (MCAO) model of focal cerebral ischemia-reperfusion was used. The rats were divided into four groups: sham control group, ischemia-reperfusion group, Sal B 1 and 10 mg x kg(-1) groups. Sal B was consecutively administrated once a day by ip injection after MCAO. The neurogenesis in SGZ and SVZ was investigated by BrdU method 7 days after MCAO. The Nissl staining for neurons in the hippocampal CA1 and cerebral cortex was performed 14 days after MCAO. A beam-walking test was used to monitor the motor function recovery. We found that brain ischemia resulted in an increase of BrdU positive cells both in ipsilateral SGZ and SVZ at 7th day after MCAO. Sal B (10 mg x kg(-1)) significantly increased further the number of BrdU positive cells both in SGZ and SVZ (P < 0.01). Ipsilateral hippocampal neuron damage occurred and CA1 almost lost 14 days after MCAO. Sal B (10 mg x kg(-1)) obviously attenuated the neuron damage and increased the number of neuron both in ipsilateral CA1 and cerebral cortex (P < 0.01). We also observed an obvious improvement of motor function recovery when Sal B (10 mg x kg(-1)) administrated. From the results above we concluded that Sal B stimulated neurogenesis process both in SGZ and SVZ after brain ischemia, and also alleviated neural cells loss and improved motor function recovery after brain ischemia in rats.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Benzofuranos
/
Daño por Reperfusión
/
Neurogénesis
/
Actividad Motora
Tipo de estudio:
Etiology_studies
Límite:
Animals
Idioma:
Zh
Revista:
Yao Xue Xue Bao
Año:
2007
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
China