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目的 探讨凋亡机制在β-淀粉样蛋白 (β- amyloid protein,Aβ)脑内致病作用中的意义。方法 用微量注射器将 Aβ1 - 4 0 注射到大鼠右侧海马 CA1 区诱发 Aβ在脑内该区域的沉积。7d后 ,用 HE染色、TUNEL法及透射电镜检测该区细胞凋亡 ;用免疫组化 SABC法检测 Bax/ Bcl- 2的表达。结果 在 Aβ组右侧海马 CA1 区 HE、TUNEL染色及电镜均发现大量凋亡细胞 ,而假手术对照组和生理盐水对照组未发现细胞凋亡 ;Aβ组 Bax表达增强 ,而Bcl- 2表达在 3组间无明显差异。结论 本研究结果表明 Aβ能诱导脑内神经元的凋亡 ,Bax高表达可能在上述凋亡机制中起一定作用 ,支持细胞参与 Alzheimer病 (Alzheimer,s Disease,AD)发病的观点。
Objective To investigate the role of apoptosis in the pathogenesis of β-amyloid protein (Aβ) in the brain. Methods Aβ1 - 40 was injected into CA1 area of the right hippocampus by microinjector to induce the deposition of Aβ in the brain. After 7 days, HE staining, TUNEL and transmission electron microscopy were used to detect the apoptosis in this area. The expression of Bax / Bcl-2 was detected by immunohistochemical SABC method. Results Apoptotic cells were found by HE staining, TUNEL staining and electron microscopy in the right hippocampal CA1 region of the Aβ group. No apoptosis was found in the sham operation group and the saline control group. The expression of Bax was increased in the Aβ group, while the expression of Bcl- No significant difference between the three groups. Conclusion The results of this study indicate that Aβ can induce neuronal apoptosis in the brain. High expression of Bax may play a role in the above mechanism of apoptosis and support the view that cells participate in the pathogenesis of Alzheimer’s disease (AD).