| Objective:The effects of allicin on proliferation, apoptosis, migration and invasion of SGC-7901cells in vitro were studied，and its mechanism was explorated preliminarily. The presentstudy provided some experimental data for studies on the anti-tumor target and clinicalapplication of allicin.Methods:Human gastric cancer cell lines SGC-7901were cultured with cell culture technology,and cells in logarithmic growth phase were taken for the experiment.1. SGC-7901cells in logarithmic growth phase were treated with allicin12,24and48h for12,24and48μg/ml respectively, MTT assay was used to detect proliferation ofSGC-7901cells, and Annexin V-FITC/PI double staining method with flow cytometrywas used to determine apoptosis of SGC-7901cells.2. Cell scratch healing method was used to detect the cell migration of SGC-7901cells, and transwell chamber assay was used to determine invasion of SGC-7901cells.3. The releases of MMP-2, HMGB-1protein from SGC-7901cells were detected byenzyme-linked immunosorbent assay (ELISA), and Western blot assay was used todetermine MMP-2, HMGB-1protein expression in SGC-7901.Results:1. At48h of SGC-7901cells treating with48μg/ml allicin, compared with controlgroup, SGC-7901cells volume became smaller, the cells were round, and accompanied by a large number of cell debris, the number of floating cells significantly increased.2. MTT assay results show that, compared with the control group, SGC-7901cellsproliferation was significantly inhibited by12,24and48μg/ml allicin at12,24and48h(P＜0.05), in concentration-dependently and time-dependently, the inhibition was alsoenhanced accordingly.3. Annexin V-FITC/PI doubling staining assay results show that, the allicin couldsignificantly promote apoptosis of SGC-7901cells, the rate of apoptosis in12,24and48μg/ml allicin groups were6.28±0.59%,11.15±0.20%﹙P <0.05﹚and30.67±2.73%﹙P <0.01﹚respectively in a dose-dependent manner, compared with3.95±1.45%in control group.4. Scratch Wound Healing assay results show that, the allicin could significantlyinhibit the migration of SGC-7901cells. Compared with control group, the allicinsignificantly inhibited narrowing of scar width at12,24and48h after scratching (P＜0.01) in a time-dependent manner, the inhibition was most obvious at48hours.5. Transwell chamber assay results show,24h after cells being treated with12and24μg/ml allicin, the number of cells through lower chamber was66.60±2.41and31.20±2.17compared with96.80±5.07in control group, which suggested that allicincould inhibit the invasion of SGC-7901cells in a dose-dependent manner (P<0.05).6. ELISA results show that, at48h after SGC-7901cells were treated with12,24and48μg/ml allicin, MMP-2protein released from cells was24.69±0.93、17.46±1.63and5.49±1.00ng/ml compared with32.01±2.52ng/ml in control group, and HMGB-1protein released from cells was0.89±0.05、0.65±0.03and0.15±0.13ng/ml comparedwith1.32±0.14ng/ml in control group, which suggested that allicin could inhibit therelease of MMP-2and HMGB-1protein from SGC-7901cells in a dose-dependentmanner.7. Western blot analysis results show that, the expression of MMP-2and HMGB-1protein in SGC-7901cells were significantly reduced after treated with allicin of12,24 and48μg/ml(P<0.05), which suggested that the expression of MMP-2and HMGB-1protein in SGC-7901cells were inhibited in a dose-dependent manner.Conclusion:Allicin can inhibit the proliferation, migration and invasion of human gastric cancerSGC-7901cells, and induce cell apoptosis，its inhibition on invasion may be relatedwith the inhibition of MMP-2protein, and its induction on apoptosis and inhibition onmigration may be related with the down-regulation of HMGB-1protein. |
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