摘要
目的探讨β-淀粉样蛋白(β-amyloid peptide,Aβ)毒性对大鼠海马神经元的损伤以及JNK信号转导通路在此过程中的作用。方法应用Aβ1-40注射大鼠双侧海马CA1区建立毒性损伤模型,通过HE染色、Nissl染色、TUNEL染色、免疫组化法、透射电镜并结合图像分析技术研究海马的病理学变化以及神经元的存活与凋亡、超微结构及p-JNK阳性细胞率。结果与对照组比较,大鼠注射Aβ后,海马CA1区锥体细胞排列松散,数目减少,神经元固缩、浓染,胶质细胞明显增生,超微结构可见明显凋亡特征,TUNEL阳性细胞数明显增多(P<0.01),p-JNK阳性细胞比例明显升高(P<0.01)。结论 Aβ可明显诱导海马神经元凋亡,JNK信号转导通路参与了Aβ的神经毒性损伤作用。
Aim To investigate the hippocampal neuronal injury induced by β-amyloid peptide （ Aβ） in rats and the candidate contribution of JNK signal transduction pathway to Aβ toxicity. Methods Rats were bilaterally injected with Aβ1 -40 into hippocampi CA1 area. The pathological changes,survival and apoptosis,and ultrastructure of hippocampal neurons,as well as p-JNK positive cells were observed by HE staining,Nissl staining,TUNEL staining,immunohistochemistry and transmission electron microscopy,respectively. Results Thepyramidal cells in hippocampus arranged loosely with decreased cell number. The gliacytes significantly proliferated. Significant apoptotic features were observed in CA1 ultrastructure. TUNEL-positive cells and p-JNK-positive cells significantly increased （ P〈0. 01） . Conclusions Aβ can significantly induce neuronal apoptosis in hippocampus in rats. JNK signal transduction pathway participates Aβ neuronal toxicity of apoptotic injury.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2010年第8期1034-1037,共4页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No30701102
30830188)
