Abstract:

Objective To investigate the effect and mechanism of allicin combined with 5-FU on proliferation inhibition and apoptosis of the mucoepidermoid carcinoma MEC-1 cell line in mucoepidermoid carcinoma in order to provide the corresponding basis for subsequent clinical drug application. Methods MEC-1 cells in the logarithmic growth phase were randomly divided into control groups and experimental groups. The control groups were PBS groups containing 0.1% DMSO, while the experimental groups were the allicin group, 5-FU group and combined drug group (the allicin combined with the 5-FU group). The proliferation inhibition rates of allicin, 5-FU and allicin combined with 5-FU in MEC-1 cells were detected by the CCK8 method at different concentrations (0, 25, 50, and 75 mg/L) for 24 h, and the IC₅₀ value of allicin and 5-FU after 24 hours was calculated. The apoptotic rate of MEC-1 cells treated with allicin, 5-FU and allicin combined with 5-FU at different concentrations (0, 25, 50, and 75 mg/L) for 24 hours was measured by flow cytometry. The expression of Bax and Bcl-2 protein was determined by Western blot analysis of the IC₅₀ concentration of allicin and 5-FU alone and in combination with MEC-1 cells for 24 hours. Results The growth inhibition rate and apoptosis rate of MEC-1 cells in the combined drug group were higher than those in the allicin group and the 5-FU alone group (P < 0.01). Allicin and 5-FU alone and in combination downregulated Bcl-2 protein and upregulated Bax protein expression, and the combined drug group had the largest ratio of Bax/Bcl-2 (P < 0.05). Conclusion Allicin and 5-FU both alone and in combination can inhibit the proliferation of and induce apoptosis in MEC-1 cells, and allicin can enhance the apoptosis of 5-FU in MEC-1 cells, which may be related to the apoptosis of the mitochondrial pathway.

Key words: mucoepidermoid carcinoma, allicin, 5-FU, proliferation, apoptosis, Bcl-2 protein, Bax protein