Reversal Effect of Dihydromyricetin on Multiple Drug Resistance in SGC7901/5-FU Cells

Document Type : Research Articles


1 Department of Biochemistry, Wannan Medical College, Wuhu, Anhui, P.R.China.

2 Anhui Province Key Laboratory of Active Biological Macromolecules, Wuhu, Anhui, P.R.China.

3 Wuhu second Sanatorium for Retired Cadres, Anhui military area, Wuhu, Anhui, P.R. China.

4 Encephalopathy Center, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, P.R. China.


Background: One of the most common treatment for gastric cancer is chemotherapy, however, multiple drug resistance (MDR) induce the therapeutic effect which result in the failure of anticancer therapy. Dihydromyricetin (DMY) was reported to have antitumor activities on various human cancer cells in vitro, our previous studies demonstrated that DMY combined with mitomycin has inhibitory effect on proliferation of gastric carcinoma cells. However, the underlying role of DMY reversing the MDR of gastric carcinoma is poor understood. The aim of this study was to evaluate the reversal effect of DMY on MDR and investigate the molecular mechanisms in vitro. Methods: Using MTT assay, we identified the toxicity of DMY on SGC7901 and SGC7901/5-FU cells. The effect of DMY on 5-FU induced apoptosis was evaluated by flow cytometry analysis. Using RT-PCR and Western blot, we determined the MDR1 mRNA and protein expression. Results: DMY induced growth inhibition in both SGC7901 and SGC7901/5-FU cells, the IC50 value was 13.64±1.15 µg/mL, 20.69±1.82 µg/mL respectively. DMY treatment sensitized SGC7901/5-FU cells to cytotoxicity of 5-FU. The combination of DMY with 5-FU increased the apoptosis rate (9.91%, 16.67%) comparing with 5-FU alone (5.25%). Comparing with the control group, the MDR1 mRNA and protein expression in SGC7901/5-FU cells after treatment of DMY decreased significantly (P< 0.05). Conclusion: In brief, our study demonstrated that DMY effectively reversed multi-drug resistance occurring in SGC7901/5-FU cells cultured in vitro, and the potential mechanism was involved in the downregulation of the MDR1 expression.


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