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CJAP ›› 2017, Vol. 33 ›› Issue (5): 385-390.doi: 10.12047/j.cjap.5565.2017.093

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Effects of dihydroartemisinin on radiosensitivity of Raji cells

ZHANG Lei2, CHENG Long-qiu2, ZHOU Zhao3, Lv Lin-lin1, LIU Ge-xiu1   

  1. 1. Insitute of Hematology, Jinan University, Guangzhou 510632, China;
    2. Department of Bioengineering, Jinan University, Guangzhou 510632, China;
    3. Key Laboratory for Regenerative Medicine of Ministry of Education, Jinan University, Guangzhou 510632, China
  • Received:2017-02-13 Revised:2017-05-31 Online:2017-09-28 Published:2018-06-19
  • Supported by:

Abstract: Objective: To study the effects of dihydroartemisinin (DHA) on radiation sensitivity of Raji cells, and explore its mechanisms.Methods: CCK8 was used to determine the effect of DHA on cell viability of Raji cells; apoptosis, intracellular reactive oxygen speies(ROS) and mitochondrial membrane potential of Raji cells were detected by flow cytometry; and the protein expressions of protein kinase B(AKT), phospho-rylated-protein kinase B(p-AKT), Bcl-2 and Bax were determined by Western blot.Results: The cells were randomly divided into four groups:control group, DHA(5μmol/L DHA), irradiation(IR, 4 Gy), IR+DHA group (4 Gy IR+5 μmol/L DHA). Compared with the other three groups, cells in DHA+IR group exhibited lower mitochondrial membrane potential (P<0.01). While the intracellular ROS content and apoptosis rate of Raji cells in DHA+IR group were increased significantly(P<0.01). In addition, compared with the other three groups, there was no significant difference in the expression of AKT, but the phosphorylation of AKT protein were significantly inhibited and the expression of Bcl-2 protein was markedly decreased. However, the expressions of Bax and Cleaved-Caspase-3 protein were markedly increased.Conclusion: DHA might activate the mitochondrial apoptotic signal via inhibiting phosphoinositide 3-kinase (PI3K/AKT) pathway and increase oxidative stress to enhance the radiosensitivity of Raji cells.

Key words: dihydroartemisinin, Raji cells, mitochondrial apoptotic signal, PI3K-AKT signal pathway

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