Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (19): 3518-3521.doi: 10.3969/j.issn.1673-8225.2011.19.022

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Effect of arsenic trioxide on multi-drug resistance of HL60/ADR cells

Huang Ming1,2, Meng Fan-yi1, Cai Yan-xia1, Wang Zhi-xiang1, Xia Li-hua2, Chen Jia-bin2   

  1. 1Hematology Department, Nanfang Hospital of Southern Medical University, Guangzhou  510515, Guangdong Province, China
    2Guangdong Prevention and Treatment Center for Occuptional  Diseases, Guangzhou  510300, Guangdong Province, China
  • Received:2011-02-17 Revised:2011-04-02 Online:2011-05-07 Published:2011-05-07
  • Contact: Meng Fan-yi, Master, Professor, Hematology Department, Nanfang Hospital of Southern Medical University, Guangzhou 510515, Guangdong Province, China mengfu@medmail.com.cn
  • About author:Huang Ming☆, Doctor, Attending physician, Hematology Department,Nanfang Hospital of Southern Medical University, Guangzhou 510515, Guangdong Province, China; Guangdong Prevention and Treatment Center for Occuptional Diseases, Guangzhou 510300, Guangdong Province, China echo.echo@126.com
  • Supported by:

    Guangdong Science and Technology Planning Project, No. 2007B031515005*

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Abstract:

BACKGROUND: The treatment of arsenic trioxide (As2O3) on acute promyelocytic leukemia (APL) has acquired good effect.
OBJECTIVE: To investigate the effect and mechanism of As2O3 on reversing multidrug resistance of HL60/ADR cell line.
METHODS: HL60/ADR cells were divided into control group and As2O3 group. Cells of control group were incubated with nun-drug, those of As2O3 group incubated with 48-hour IC50 As2O3.
RESULTS AND CONCLUSION: As2O3 could enhance the intracellular accumulation of DNR and decrease the expression of MRP1 in HL60/ADR cells (P < 0.05). At the same time, the early and late apoptosis rate of HL60/ADR cells both increased significant with time-dependently, which was higher than that in the control group (P < 0.01). As2O3 could also elevate the expression of bax, caspase-3, caspase-9, PARP, and decelerate the expression of Bcl-2, NF-κB p65, p-p65.

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