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目的:观察不同时点分别结扎左、右颈总动脉建立大鼠血管性痴呆模型中海马CA1区神经元凋亡和Bcl-2及Bax蛋白表达的影响,探讨其在血管性痴呆发病过程中的作用。方法:采取间隔3 d分2次结扎双侧颈总动脉建立血管性痴呆模型,术后4周用TUNEL法检测海马CA1区神经元凋亡,用免疫组织化学法检测其Bcl-2及Bax蛋白表达。结果:模型组大鼠海马CA1区可见大量凋亡神经元;模型组Bcl-2及Bax蛋白表达明显增加,与假手术组比较差异均有显著意义(P<0.05)。结论:此血管性痴呆模型大鼠中海马CA1区神经元大量凋亡丢失,可能是导致血管性痴呆的病理基础。
OBJECTIVE: To observe the effects of left and right common carotid artery ligation at different time points on the neuronal apoptosis and the expression of Bcl-2 and Bax in hippocampal CA1 area of vascular dementia model in rats, and to explore its role in the pathogenesis of vascular dementia effect. Methods: Vascular dementia models were established by ligating bilateral common carotid arteries at 3 d intervals. Neuronal apoptosis was detected by TUNEL method in hippocampal CA1 area 4 weeks after operation. The expression of Bcl-2 and Bax protein was detected by immunohistochemistry expression. Results: A large number of apoptotic neurons were found in hippocampal CA1 region of rats in model group. The expression of Bcl-2 and Bax in model group was significantly increased compared with sham operation group (P <0.05). Conclusion: A large number of apoptotic neurons in hippocampal CA1 region of rats with vascular dementia were lost, which may be the pathological basis of vascular dementia.