摘要
目的探讨非促分裂酸性成纤维细胞生长因子(nmaFGF)对放线菌素D(ActD)诱导Balb/c3T3成纤维细胞凋亡的保护作用。方法利用放线菌素D诱导3T3细胞凋亡的模型,将实验分为空白对照组、ActD处理组和nmaFGF处理组,采用DNA琼脂糖凝胶电泳和流式细胞仪两种分析方法测定nmaFGF对3T3细胞凋亡的影响。并利用Western免疫印迹检测nmaFGF作用于3T3细胞后Akt信号通路中p-Akt分子的表达。结果空白对照组的凋亡率为1.53%;ActD处理组3T3细胞发生明显的细胞凋亡,凋亡率为33.83%;而nmaFGF处理组的细胞凋亡受到显著抑制,凋亡率分别下降到18.97%,15.17%和12.83%,凋亡下降率分别为14.86%,18.66和21.00%。Western半定量检测结果显示,在0.1~10μg/ml的浓度下,随着nmaFGF剂量的增加,p-Akt的表达水平有所增加,3T3细胞的凋亡率随之下降。结论nmaFGF可以通过AKT途径显著抑制由放线菌素D诱导的Balb/c成纤维细胞的凋亡。
Objective To investigate the anti-apoptosis effect of nonmitogenie acidic fibroblast growth factor on balb/c 333 fibroblast apoptosis induced by AetD. Methods Using AetD to establish 333 fibroblast apoptosis models, the experimental groups included:①control, ②AetD only, ③nmaFGF and ActD. The apoptcsis of 333 fibroblasts induced by ActD was examined by DNA fragmentation and flow cytometry(FCM) ; the expression of phosphor-Akt protein was detected by Western blot. Results AetD induced apoptosis in 3T3 fibrohlasts. The percentage of apoptosis 3T3 fibrohlast was significantly lower in groups pretreated with nmaFGF than the groups treated with ActD only. And it showed increased antagonistic effect of nmaFGF on 333 fibroblast apopwsis in 0. 1, 1 and 10μg/ml nmaFGF pretreated groups, Furthermore, addition of nmaFGF to 333 cells significandy increased Akt phosphorylation. Conclusion Nonmitogenic acidic fibroblast growth factor can significantly inhibit the apopwsis of the Balb/c 3T3 fibroblast cells induced by ActD.
出处
《广东医学》
CAS
CSCD
北大核心
2006年第2期167-169,共3页
Guangdong Medical Journal
基金
国家"863"基金资助项目
国家"863"重大专项(编号2002AA2Z3318及2001AA215131)