CAJ | 학술논문

目的研究丁基苯酞(NBP)对血管性痴呆(VD)大鼠记忆、海马病理变化及抗凋亡蛋白(Bcl-2)和促凋亡蛋白(Bax)蛋白表达的影响.方法采用永久性结扎双侧颈总动脉方法制备VD大鼠模型.SD大鼠被随机分成假手术组、VD模型组、NBP治疗组、尼莫地平治疗组.应用Morris水迷宫检测大鼠记忆能力,苏术精-伊红(HE)染色观察海马神经元形态,免疫组化检测海马Bcl-2和Bax的表达.结果 VD模型组与假手术组大鼠比较记忆能力显著下降,逃避潜伏期分别为(78.79±21.93) s与(16.96±7.44) s (P＜0.05),海马神经元病理改变严重,免疫阳性细胞数量显著增加,其中Bax变化更为显著 (43.00±6.72与6.00±1.29,P＜0.05),Bcl-2与Bax的比值较对照组明显降低;NBP治疗组与模型组比较记忆能力显著改善,逃避潜伏期分别为(47.13±21.75) s与(78.79±21.93) s (P＜0.05),海马神经元病理形态明显改善,Bcl-2免疫阳性细胞数显著增多(33.14±8.05与21.81±4.97,P＜0.05),Bax免疫阳性细胞数显著减少(32.93±4.99与43.00±6.72,P＜0.05).NBP治疗组与尼莫地平治疗组之间比较,各项指标均无显著差异 (P＞0.05).结论 NBP能改善VD大鼠记忆能力,抑制海马细胞凋亡,对VD大鼠有一定的治疗作用.
목적 연구정기분태(NBP)대혈관성치태(VD)대서기억、해마병리변화급항조망단백(Bcl-2)화촉조망단백(Bax)단백표체적영향.방법 채용영구성결찰쌍측경총동맥방법제비VD대서모형.SD대서피수궤분성가수술조、VD모형조、NBP치료조、니막지평치료조.응용Morris수미궁검측대서기억능력,소술정-이홍(HE)염색관찰해마신경원형태,면역조화검측해마Bcl-2화Bax적표체.결과 VD모형조여가수술조대서비교기억능력현저하강,도피잠복기분별위(78.79±21.93) s여(16.96±7.44) s (P＜0.05),해마신경원병리개변엄중,면역양성세포수량현저증가,기중Bax변화경위현저 (43.00±6.72여6.00±1.29,P＜0.05),Bcl-2여Bax적비치교대조조명현강저;NBP치료조여모형조비교기억능력현저개선,도피잠복기분별위(47.13±21.75) s여(78.79±21.93) s (P＜0.05),해마신경원병리형태명현개선,Bcl-2면역양성세포수현저증다(33.14±8.05여21.81±4.97,P＜0.05),Bax면역양성세포수현저감소(32.93±4.99여43.00±6.72,P＜0.05).NBP치료조여니막지평치료조지간비교,각항지표균무현저차이 (P＞0.05).결론 NBP능개선VD대서기억능력,억제해마세포조망,대VD대서유일정적치료작용.
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.