摘要
目的 :利用体外培养的PC12表现出神经细胞的特性 ,用Aβ2 5-3 5诱导PC12细胞凋亡 ,建立神经细胞毒性作用的模型 ,来探索bFGF对Aβ2 5-3 5作用和治疗老年性痴呆 (AD)的机制。方法 :通过Giema’s、PI染色法、DNA琼脂糖凝胶电泳、Westernblot及流式细胞仪研究了加入Aβ2 5-3 5培养的以及Aβ2 5-3 5和bFGF共培养的PC12细胞的形态和分子生物学改变及凋亡相关基因Bcl- 2 ,Bax表达的变化。结果 :Aβ2 5-3 5可诱导PC12细胞核DNA发生降解 ,出现染色质浓缩成块状、胞浆浓缩、胞膜内陷、凋亡小体形成等 ;而Aβ2 5-3 5和bFGF共培养的PC12细胞则能缓解这种形态学上的变化 ,细胞凋亡率减少 ,Bcl- 2的表达量上调而Bax的表达量下调。结论 :bFGF能抑制Aβ2 5-3 5对神经细胞的毒性作用 ,其机制可能是通过调控Bcl- 2、Bax的表达来实现的。
AIM: To clarify the effect of bFGF on the neurotoxity of Aβ 25-35 in PC12 cells and its potential application in the treatment of Alzheimer's disease. METHODS: Giema's, PI stainning, DNA agarose gel electrophoresis, Western blot and FCM were used to detect the morphological and biochemical changes of cultured PC12 cells treated with Aβ 25-35 and bFGF+ Aβ 25-35 , and the expression of apoptosis-related gene bcl-2, bax. RESULTS: Morphological and biochemical characteristics of apoptosis, such as internuclear DNA fragmentation, compaction of nuclear chromatin, membrane blobbing, formation of apoptotic bodies, were observed in PC12 cells treated with Aβ 25-35 . However, in PC12 cells treated with bFGF+ Aβ 25-35 , the above changes were significantly reversed, the expression of Bcl-2 was up-regulated while that of Bax was down-regulated. CONCLUSION: bFGF can inhibit the neurotoxity of Aβ 25-35 to neurons by regulating the expression of the apoptosis-related gene Bcl-2 and Bax.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第4期374-377,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目 (No .3990 0 16 8)
