CAJ | 학술논문

目的：研究埃克替尼对涎腺腺样囊性癌细胞系ACC-M细胞凋亡的影响及可能机制。方法：ACC-M细胞分为6组，即对照组，低、中、高剂量（10、20、40μmol/L）埃克替尼组，MnTMPyP组以及MnTMPyP＋埃克替尼组。采用MTT法检测各组细胞的活性， Caspase-3活力检测试剂盒检测Caspase-3蛋白的活力， DCFH-DA荧光探针检测ROS水平，Western blot检测线粒体和胞质MnSOD蛋白的表达。结果：与对照组相比，埃克替尼低、中、高剂量组细胞活性降低，Caspase-3蛋白活力增强，ROS水平升高，线粒体中MnSOD蛋白表达减少，胞质中MnSOD蛋白表达增加（P均＜0．05）；MnTMPyP能拮抗上述变化（P均＜0．05）。结论：埃克替尼可能通过ROS介导的MnSOD线粒体转位诱导ACC-M细胞凋亡。
목적：연구애극체니대연선선양낭성암세포계ACC-M세포조망적영향급가능궤제。방법：ACC-M세포분위6조，즉대조조，저、중、고제량（10、20、40μmol/L）애극체니조，MnTMPyP조이급MnTMPyP＋애극체니조。채용MTT법검측각조세포적활성， Caspase-3활력검측시제합검측Caspase-3단백적활력， DCFH-DA형광탐침검측ROS수평，Western blot검측선립체화포질MnSOD단백적표체。결과：여대조조상비，애극체니저、중、고제량조세포활성강저，Caspase-3단백활력증강，ROS수평승고，선립체중MnSOD단백표체감소，포질중MnSOD단백표체증가（P균＜0．05）；MnTMPyP능길항상술변화（P균＜0．05）。결론：애극체니가능통과ROS개도적MnSOD선립체전위유도ACC-M세포조망。
Aim:To observe the effect and mechanism of icotinib on the apoptosis induction of the salivary adenoid cystic carcinoma-M( ACC-M) cells.Methods:ACC-M cells were allocated into control group ,low-,median-,high-concen-tration(10,20,40 μmol/L) icotinib-treatment groups,MnTMPyP group and MnTMPyP +icotinib group.The cell viability of ACC-M was measured by MTT assay .The expression of Caspase-3 was assessed by Caspase-3 activity detection kit .The lev-el of ROS was assayed by the fluorescent probe using DCFH-DA.The expression of MnSOD in mitochondrion was deter-mined by Western blot analysis .Results:Compared with control group ,the cell viability of ACC-M significantly decreased in low-,median-,high-concentration icotinib groups ,the expressions of Caspase-3 and ROS increased ,the expression of Mn-SOD significantly decreased in mitochondrion while increased in cytoplasm (all P<0.05).However,MnTMPyP reversed the effects of icotinib(all P<0.05).Conclusion:Icotinib may induce apoptosis of ACC-M cells through ROS-mediated Mn-SOD mitochondrial translocation .