中文摘要：

目的：探讨酪氨酸蛋白激酶抑制剂盐酸埃克替尼（Icotinib）对人非小细胞肺癌（NSCLC）HCC827细胞Akt通路的活化和凋亡相关蛋白PARP、Caspase-3和Caspase-8表达的影响。方法：将体外培养的人肺癌HCC827细胞分为Icotinib处理组和未处理的对照组，采用四甲基偶氮唑盐法（MTT）检测Icotinib对细胞增殖的抑制作用，采用Westernblot检测蛋白表达，应用SPSS13．0进行统计学分析。结果：Icotinib处理HCC827细胞48h的IC50为0．65μmoL／L；选用0．001、0．01μmol／L和0．1μmol／L的Icotinib分别作用HCC827细胞48h，细胞凋亡率分别为（3.35±1．77）％、（8．95±3．18）％和（20．4±3．12）％（P〈0．05）。与对照组相比，Icotinib明显抑制Akt的磷酸化水平，诱导PARP、Caspase-3和Caspase-8活化裂解。结论：Icotinib通过抑制Akt信号通路的活化、进一步诱导PARP、Caspase-3和Caspase-8裂解，进而抑制人NSCLC细胞增殖及诱导细胞凋亡。

英文摘要：

Objective：To explore the effects of Icotinib on the activation of Akt and the expressions of apoptosis - related proteins in human non - small cell lung cancer cells （NSCLC）. Methods： Cell proliferation was measured using MTT assay. The expressions of proteins were detected by Western blot. All experimental data were analyzed with SPSS （13.0 soft）. Results： Icotinib significantly inhibited HCC827 cell viability and the eoncertration of inhibited cell viability （ IC50 ） for 48h was 0.65 μmol/L. After treatment with 0. 001,0.01 μmol/L and 0.1 μmol/L Icotinib for 48h, the rates of cell apoptosis were （3.35 ± 1.77 ） %, （ 8.95 ± 3.18 ） % and （20.4 ± 3.12）, respectively. Icotinib could upregulated the expression of cleavage of Caspase - 8, Caspase - 3 and PARP. After treated 24 h, Icotinib could obviously decrease the expressions of the phosphorylated Akt in HCC827 cells. Conclusion： Ieotinib inhibited the activation of the Akt signaling pathway, which consequently upregulated the split of the cleavage of Caspase - 8, Caspase -3 and PARP proteins in HCC827 cells.