Mechanism investigation of magnolol on proliferation and apoptosisof gastric cancercells

Objective To investigatethemechanismofmagnolol on proliferation and apoptosis of gastric cancer cells. Methods SGC-7901 cells werecultured with 0 (control), 20, 40, 80 μmol/Lmagnolol for 48 hrespectively. Cell viability was measured by using MTT assay. Cell apoptosis and Cell cycle was measured by usingflow cytometry. The expression of B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), cysteinyl aspartate specific proteinase 3 (cleaved caspase 3 ), CyclinD1, CyclinE and cyclin dependent kinase 2 (CDK2) protein were measured by western blotting. All the data were analyzed by using SPSS 17.0 software. Measurement data, including cell proliferation inhibition rate, cell apoptosis, cell cycle and protein expression, were expressed as (±s), and were examinedby using t test. A P value<0.05 was considered as statistically significant difference. Results Compared with control group, SGC-7901 cells with 20, 40, 80 μmol/L magnolol, exhibited decreased cell viability, increased apoptotic rate, arrested in the G1 phage, with down-regulated expression of Bcl-2, CyclinD1, CyclinE and CDK2, and up-regulated expression of Bax, cleaved caspase 3 (P<0.01). Conclusion Magnolol could inhibit SGC-7901 cells proliferation and induce cell apoptosis via regulation the expression of cell cycle protein and cell apoptotic related protein. Key words: Stomach neoplasms; Cell proliferation; Apoptosis; Magnolol