Effect of allicin on THP-1, MT-2 and WISH cell apoptosis induced by vesicular stomatitis virus (VSV) and the molecular mechanism involved
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.