ZHAO Xinª²Han, WANG Zhiª²Yu, LI Jing, QUAN Ping

    Department of Oncology, First Affiliated Hospital, Medical College, Xi¬ðan Jiaotong University, Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Xi¬ðan 710061, China

    ¡¾Abstract¡¿AIM: To study whether bclª²2 antisense oligodeoxynucleotides(ASON) can enhance the apoptosisª²inducing effects of artesunate on human chronic granulocytic leukemia K562 cell strain. METHODS: Bclª²2 ASON was synthesized and transfected into K562 cells with liposome, and its expression was detected by Western blotting method. The terminal deoxynucleotidyl transferaseª²mediated dUTP nick end labeling (TUNEL) and flow cytometry (FCM) were applied to detect cell apoptosis. RESULTS: Bclª²2 ASON could obviously silence bclª²2 expression in K562 cell strain. Within the range of 1ª²7 mg/L, artesunate obviously inhibited K562 cell proliferation in a timeª² and doseª²dependent manner, and 7 mg/L artesunate which affected K562 cells for 72 h had the lowest A value. TUNEL showed that K562 cells became smaller and the nuclei presented one or many condensed chromatin masses, compared to K562 cells which were not transfected with bclª²2 ASON, bclª²2 ASON transfected K562 cells were more sensitive to artesunate; the apoptosis peak of lower subª²diploid DNA content in G1 phase was observed in FCM, and apoptosis of K562 cells induced by artesunate mainly occurred in G1/S phase; compared to K562 cells which were not transfected with bclª²2ASON, bclª²2 ASONª²K562 cell apoptosis rate was significantly higher. CONCLUSION: Artesunate could induce the apoptosis of K562 cells within a certain dose range in vitro, and bclª²2 ASON could enhance the apoptosisª²inducing effect of artesunate. ......