【摘要】 目的:观察缺血预处理能否对大鼠缺血再灌注后海马CA1区神经元凋亡起拮抗作用,并探讨p53基因在其中的作用。方法:复制全脑缺血再灌注及缺血预处理模型,利用HE染色,流式细胞仪,RT-PCR和免疫组化方法检测海马CA1区锥体细胞形态学变化、神经元凋亡百分率及p53基因表达。结果:缺血预处理(IPC)组的神经元存活数目[(217±9)/0.72mm2]明显高于单纯缺血再灌注(IR)组[(29±5)/0.72mm2],P<0.01;IPC组的凋亡百分率(2.07%±0.21%)显著低于IR组(4.26%±0.08%),P<0.01;IPC组p53基因表达显著弱于IR组。结论:缺血预处理可通过抑制p53基因表达,从而抑制大鼠海马神经元凋亡,对缺血神经元起保护作用。更多还原

【Abstract】 AIM: To examine whether ischemic preconditioning (IPC) can protect against apoptosis in CA1 subfield of hippocampus following reperfusion of a lethal ischemia in rats and explore the role of IPC by inhibiting the expression of p53 in this process. METHODS: Wistar rats were used in the experiment. A global ischemia/reperfusion model was induced by 4-vessel occlusion. The rats were divided into the following three groups randomly: (1) ischemic preconditioning group (IPC group); (2) ischemia/reperfusion group (IR group); (3) control group. The histopathological changes, the percentage of apoptosis and the expression of p53 gene in CA1 region of rat hippocampus were examined by HE staining, FCM, RT-PCR and immunohistochemistry techniques. RESULTS: The neuronal density of CA1 region in IPC group [(217±9)/0.72 mm2] was significantly higher than that in IR group [(29±5)/0.72 mm2, P<0.01]. The percentage of apoptotic neurons in IPC group (2.07%±0.21%) was lower than that in IR group (4.26%±0.08%), P<0.01. Compared with IR group, the expression of p53 gene in IPC group was significantly weakened. CONCLUSION: Ischemic preconditioning protects the ischemic neurons in CA1 region of rat hippocampus by inhibiting the expression of p53 gene.更多还原