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 ana-lyze the cell apoptosis after exposed to carvacrol. Transwell assay was used to analyze the effect of carvacrol on cell metastasis. Quanti-tative realtime-PCR was used to detect the expression of MMP-9 and TIMP-1. The expression of caspase-9 and PARP,and the activa-tion 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-1 vs 20 μmol·L-1 ,P<0. 000 1;0 μmol·L-1 vs 40 μmol·L-1 ,P<0. 000 1;0 μmol·L-1 vs 80μmol·L-1 ,P<0. 000 1)and the invasion ability was decreased(0 μmol·L-1 vs 80 μmol·L-1 ,P<0. 000 1). The expression of caspase-9(0 μmol·L-1 vs 80 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 signa-ling 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.