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Journal of Guangzhou University of Traditional Chinese Medicine ; (6): 969-973, 2014.
Artigo em Chinês | WPRIM | ID: wpr-485432

RESUMO

Objective To investigate the effect of the dihydroartemisinin (DHA) on the human low-differentiated lung adenocarcinoma cell line A549 and to explore its mechanism. Methods The A549 cells at logarithmic growth phase were divided into control group and DHA group. The cells in the control group were incubated with conventional reagent, and the cells in DHA group were incubated with 500 nmol/L of DHA. After incubation for 72 hours, methyl thiazolyl tetrazolium (MTT) assay was used to examine the proliferation of A549 cells in the two groups. Gene expression of p85, Akt, Bax and Bcl-2 was detected by real-time fluorescence quantitative polymerase chain reaction (PCR) . The protein expression of p85, Akt, p-p85, p-Akt, Bax and Bcl-2 was detected by Western blotting method. The activity of Caspase3 was measured by Caspase3 colorimetric assay kit. Results Compared with the control group, the proliferation rate of A549 cells in DHA group was significantly decreased ( P0.05), but p-p85, p-Akt and Bcl-2 protein expression levels were significantly decreased ( P<0.01) , and Bax protein expression was increased ( P<0.01). Moreover, the activity of Caspase3 was also enhanced ( P<0.001). Conclusion DHA can reduce the proliferation of A549 cells and increase the apoptosis of A549 cells, and its mechanism probably has relationship with the inhibition of PI3K/Akt signaling pathway.

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