锰超氧化物歧化酶模拟化合物通过Fas途径诱导白血病K562细胞凋亡

目的：探讨锰超氧化物歧化酶模拟化合物（mi mics of manganese superoxide dismutase,MnSODm）对人白血病K562细胞的凋亡诱导效应及作用机制。方法：应用MTT比色法、An-nexin V/PI双标记和细胞形态学法观察细胞凋亡;流式细胞术（FCM）测定Fas蛋白表达水平;RT-PCR检测Caspase-3mRNA的表达水平,比色法测定Caspase-3活性变化。结果：MnSODm作用后K562细胞的增殖受到抑制,Annexin V/PI染色显示凋亡细胞明显增多,透射电镜观察呈现典型的凋亡形态改变。同时,Fas蛋白表达水平显著增高,Caspase-3mRNA表达水平明显升高,活性显著增强。结论：MnSODm可能通过Fas途径诱导白血病K562细胞凋亡。

MnSODm induces apoptosis in leukemia K562 cells through Fas-dependent pathway

AIM：To investigate the apoptosis of human leukemia cell line K562 induced by mimics of manganese superoxide dismutase（MnSODm）in vitro and the possible molecular mechanisms.METHODS：The apoptosis in K562 cells was examined by MTT colorimetric method,FITC-Annexin V and propidium iodide（PI）double staining and morphological changes method,the expression level of Fas protein was measured with flow cytometry（FCM）,and the mRNA expression and the activity of Caspase-3 were detected by RT-PCR and colorimetric assay,respectively.RESULTS：After administration with MnSODm,the proliferation of K562 cells was obviously inhibited,the cellular apoptosis was markedly enhanced with Annexin V/PI staining and the cells showed the typical apoptotic morphological changes.The expression of Fas protein in K562 cells up-regulated greatly,which accompanied with the significant increase of both mRNA expression and activity of Caspase-3.CONCLUSION：The apoptosis of leukemia K562 cells induced by MnSODm may involved in the Fas death receptor pathway.