ABSTRACT Objective: To investigate the anti proliferation effect of carvacrol on human gastric cancer cell BGC-823 and explore the molecular mechanism. Methods: The proliferation of BGC-823 cells was evaluated by MTT assay. Flow cytometry was used to analyze the cell apoptosis after exposed to carvacrol. Transwell assay was used to analyze the effect of carvacrol on cell metastasis. Quantitative realtime PCR was used to detect the expression of MMP-9 and TIMP-1. The expression of caspase-9 and PARP, and the activation of ERK and P38 were detected by Western blot. Results: The incubation with carvacrol resulted in a significant inhibition of BGC-823 cell proliferation. After the treatment with carvacrol, the apoptotic rate was significantly increased(0 μmol·L-1 vs 10 μmol·L-1,P<0.000 1;0 μmol·L-1vs 20 μmol·L-1,P<0.000 1;0 μmol·L-1vs 40 μmol·L-1, P<0.000 1;0 μmol·L-1vs80 μmol·L-1, P<0.000 1)and the invasion ability was decreased (0 μmol·L-1vs 80 μmol·L-1, P<0.000 1).The expression of caspase-9(0 μmol·L-1vs80 μmol·L-1,P<0.000 1)and TIMP-1 was increased(P<0.000 1), PRAP fragment occurred (P<0.000 1)and P38 signaling pathway was activated in the carvacrol treated group, while the expression of MMP-9 activity of ERK signaling pathway was inhibited(P<0.000 1).Conclusion: Carvacrol can inhibit cell growth and invasion, and induce cell apoptosis, which is closely related to MAPK signaling pathway. |