摘要
利用常规的HL 60细胞和转染了bcl 2基因的HL 60 /Bcl 2细胞及转染了空载体的对照HL 60 /neo细胞 (含新霉素抗性基因neo)为模型 ,研究Caspase 3及过表达的Bcl 2对凋亡过程中的各种生化、形态学特征的影响 ,探讨了Caspase 3及Bcl 2在三尖杉酯碱 (HT)诱导的HL 60细胞凋亡中的作用 .研究表明 :Caspase 3的活化在HT诱导的HL 60细胞凋亡中处于关键地位 ,导致了质膜出泡、PS翻转、染色质凝集、DNA断裂及凋亡下游事件的发生 ,而Bcl 2则通过抑制Caspase 3的活化抑制了凋亡的发生 .同时还证明 ,在HT诱导的HL 60细胞凋亡中 ,通常被认为是凋亡早期特征的磷脂酰丝氨酸 (PS)翻转并不是一个早期特征 ,它至少晚于Caspase 3的活化 。
With the model of Common HL 60 cell and those transfected with bcl 2 gene and empty vector including anti neo gene, the effect of Caspase 3 and overexpressed Bcl 2 on apoptotic biochemical and morphological character is studied in order to discus the function of Caspase 3 and Bcl 2 on apoptosis of HL 60 induced by HT. Results show that Caspase 3 activation is the central event for initiating the execution process of HT induced apoptosis in HL 60 cells. The activated Caspase 3 induces downstream apoptosis related events, including phosphatidylserine externalization, plasma membrane blebbing, chromatin condensation and DNA fragmentation etc.. Overexpression of Bcl 2 in HL 60 cells can prevent all of these events by inhibiting the activation of Caspase 3. Present research also proved that though PS externalization is always regarded as one early character of apoptosis it comes after the activation of Caspase 3 and even later than plasma membrane blebbing or chromatin condensation.
出处
《北京师范大学学报（自然科学版）》
CAS
CSCD
北大核心
2000年第6期810-816,共7页
Journal of Beijing Normal University(Natural Science)
基金
国家自然科学基金重点资助项目!(39730 16 0 )
教育部博士点基金资助项目!(19990 0 2 710 )
关键词
BCL-2
CASPASE-3
细胞凋亡
HT诱导
动物细胞
apoptosis
HL-60(neo/Bcl-2)
HT(harringtonine)
Bcl-2
Caspase-3
membrane blebbing
PS externalizatio\
