中文摘要：

目的 观察IFN-γ对AKT基因激活的小鼠髓系祖细胞系（32D细胞）的影响,探讨IFN-γ对造血细胞增殖和凋亡双向调节的可能机制.方法 用质粒转导技术使32D细胞高表达AKT基因,以IFN-γ作用32D细胞,用水溶性四氮唑（WST-1）细胞增殖检测法检测细胞增殖水平,流式细胞术检测细胞凋亡率,Western blot法检测磷酸化胞外信号调节激酶（p-Erk）1/2、信号转导和转录活化蛋白（Stat）3、p-Stat3的表达.结果 ①低浓度（100 U/ml）IFN-γ能促进32D细胞增殖、抑制凋亡,高浓度（1000 U/ml）IFN-γ则相反（100 U/ml处理24 h细胞密度为0.238±0.010;而1000 U/ml处理后为0.106±0.010,未处理组为0.170±0.010）.②低浓度IFN-γ可使32D细胞内Stat3磷酸化水平升高（1124±13）,高浓度时减低（601±13）.③转染激活型AKT质粒的32D细胞（激活型细胞）较其他组细胞的增殖率显著增高、凋亡率明显降低[分别为0.287±0.010、（9.57±0.17）%]（P＜0.05）.④激活型32D细胞较其他组细胞p-Erk1/2蛋白表达明显减低（P＜0.05）.结论 ①IFN-γ对32D细胞有双重作用,即低浓度促进细胞增殖、抑制凋亡,高浓度抑制细胞增殖、促进凋亡.②IFN-γ对32D细胞的双重效应可能是通过Stat3的磷酸化水平的增减实现的.③激活型AKT能明显促进32D细胞增殖、抑制凋亡,IFN-γ可通过调控AKT来调节细胞增殖及凋亡.④AKT激活后可以抑制Erk信号通路,可能是通过抑制Rafl的修饰实现的.

英文摘要：

Objective To investigate the effects of activated AKT on murine myeloid precursor cells （32D cells）, and the effects of IFN-γon 32D cells and its mechanisms. Methods Plasmid transduction was used to enhance the expression of AKT on 32D cells. After the transfected cells treated with IFN-γ for 24 hours, proliferation rate was tested by WST-1, apoptosis by flow cytometry, expression of phosphorylated Erk1/2、 Stat3 and phosphorylated Stat3 was determined by Western blot. Results ①IFN-γat low concentration（ 100 U/ml） enhanced the growth and proliferation of 32D cells, while at high concentration（ 1000 U/ml） suppressed them. ②Compared with control groups, low concentration IFN-γ increased （ 1124 ± 13 ）Stat3 phosphorylation in 32D-cell , while it high concentration IFN-γdecreased（601 ± 13）. 32D cells transfected with activated Akt grew rapidly （0. 287 ± 0.010） and had a low apoptotic rate [（9.57 ± 0. 17 ）% （P 〈0.05）]. ③The expression of p-Erk1/2 in transfected 32D-cell was significantly reduced （P 〈 0. 05） .④Apoptosis rate of IFN-γ treated group was significantly decreased in transfected 32D cells （ P 〈 0. 05 ）.Conclusions IFN-γ has dual effects on 32D cells, namely, at low concentration enhanced the growth and proliferation of 32D cells, while at high concentration suppressed them. Its mechanisims is possibly through Stat3 pathway. Activated Akt can significantly promote the growth and proliferation of 32D cell and significantly inhibit apoptosis and IFN-γcan regulate cell proliferation and apoptosis through AKT. AKT activation can inhibit the Erk signal pathway, which may be affected by inhibition the medificaton of Rafl.