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Vesicular stomatitis virus (VSV) has been reported to induce apoptosis and the onset of apoptosis may play an important role in virus-associated diseases. This study was conducted in order to investigate the protective effect of the herbal constituent allicin on VSV-induced apoptosis in the human monocyte line THP-1, human T lymphocytic leukemia cell line MT-2 and human amniotic cell line WISH and to determine the possible molecular mechanism involved. The THP-1, MT-2 and WISH cells were incubated with VSV in the absence or presence of different doses of allicin (10, 25 and 50 μg/ml). To study apoptosis, the cells were assessed by MTT and annexin V-propidium iodide double-staining flow cytometry. To investigate the molecular mechanism by which allicin regulates VSV-induced THP-1, MT-2 and WISH cell apoptosis, the expression of active cleavage products of caspases 3, 6, 7 and 9 and NF-κB was analyzed by western blotting. Our results indicated that allicin did not affect the adhesion and entry of VSV into THP-1, MT-2 or WISH cells. Using different concentrations of allicin, a dose-dependent protective effect on cell apoptosis was observed. In addition, the VSV-induced expression of active cleavage products of caspases 3, 6, 7 and 9 and NF-κB in THP-1, MT-2 and WISH cells was also significantly reduced by allicin at the protein level. We concluded that allicin protects THP-1, MT-2 and WISH cells from VSV-induced apoptosis by inhibiting the activation of caspases 3, 6, 7 and 9 and NF-κB, thereby suggesting a potential protective effect for allicin against virus-associated diseases.
Key words: Allicin, vesicular stomatitis virus (VSV), apoptosis, caspases, NF-κB.