Effects of butylphthalide on memory and the apoptosis-related protein in hippocampus of vascular dementia rats
10.3760/cma.j.issn.0254-9026.2011.06.023
- VernacularTitle:丁基苯酞对血管性痴呆大鼠记忆及海马Bcl-2、Bax的影响
- Author:
Shuwen XU
;
Bensheng LIU
;
Guangsheng GAO
;
Xiahui ZHANG
;
Baoping WANG
;
Shaotong XIANG
;
Fangfang HU
- Publication Type:Journal Article
- Keywords:
Dementia,vascular;
Hippocampus;
Bcl-2-associated X protein
- From:
Chinese Journal of Geriatrics
2011;30(6):512-515
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effects of butylphthalide (NBP) on memory and apoptosis related protein as well as neuronal pathology in hippocampus of vascular dementia (VD) rats. Methods VD model was generated by the permanent occlusion of bilateral common carotid arteries in SD rats to produce the forebran ischemia. Male SD rats were randomly allocated into sham-operation group, VD model group, NBP treatment group and nimodipine treatment group. The function of memory was tested by the Morris water maze. The neuronal pathological changes and the expression of Bcl-2 and Bax proteins in the hippocampus were observed with hematoxylin-eosin (HE) staining and immunohistochemical staining, respectively. Results The impaired memory of VD rats was proved by the lengthened mean escape latency [(78.79±21.93)vs.(16.96±7.44),P＜0.05] and the neuron in hippocampus was severely damaged. The decveased ratio of Bcl-2/Bax resulted from the overexpression of Bax proteins in VD model group versus the sham-operation group [(43.00±6.72)vs.(6.00±1.29),P＜0.05]. The treatment of NBP notably improved the memory function of VD rats and reduced the hippocampus pathological injury (P＜0.05). The expression of Bcl-2 protein raised [(33.14±8.05)vs.(21.81±4.97),P＜0.05] along with reduced expression of Bax protein [(32.93±4.99)vs.(43.00±6.72),P＜0.05] after NBP treatment. However, there was no significant difference in the treatment effects between nimodipine and NBP group (P＞0.05). Conclusions NBP treatment could improve memory of VD rats and reduce the hippocampus pathological lesion by inhibiting the apoptosis related protein.
