Allicin, a major biologically active component of garlic, is produced from its inactive precursor aUiin by the enzyme alliinase. In this study, we investigated its effects on human nasopharyngeal carcinoma KB cells. A...Allicin, a major biologically active component of garlic, is produced from its inactive precursor aUiin by the enzyme alliinase. In this study, we investigated its effects on human nasopharyngeal carcinoma KB cells. After incubation for 48 h, allicin inhibited the growth of KB cells in a concentration-dependent manner with an IC50 value of （2.2±0.2） μg/mL. Incubation with allicin for 48 h caused a concentration-dependent induction of apoptosis in the concentration range of （16-48） μg/mL, and the induction of apoptosis was confirmed by the changes of mitochondrial membrane potential, F-actin contents and nuclear condensation in KB cells. Moreover, allicin concentration-dependently arrested KB cells at the S-phase of the cell cycle in the range of （16-48） μg/mL. In addition, treatment with the compound caused concentration-dependent disassembly of microtubule cytoskeleton in KB cells, which is similar to the effect of colchicine, a well-known microtubule destabilizing agent. We concluded that the abilities of allicin to inhibit the proliferation of KB cells probably relate to its apoptosis induction, cell cycle arrest and microtubule destabilizing properties.展开更多
基金Grant of Modernization and Industrization of Weiur Medicine (Grant No. 2007BAI30B02-4)the grant from State Key Laboratory of Natural and Biomimetic Drugs, Peking University
文摘Allicin, a major biologically active component of garlic, is produced from its inactive precursor aUiin by the enzyme alliinase. In this study, we investigated its effects on human nasopharyngeal carcinoma KB cells. After incubation for 48 h, allicin inhibited the growth of KB cells in a concentration-dependent manner with an IC50 value of （2.2±0.2） μg/mL. Incubation with allicin for 48 h caused a concentration-dependent induction of apoptosis in the concentration range of （16-48） μg/mL, and the induction of apoptosis was confirmed by the changes of mitochondrial membrane potential, F-actin contents and nuclear condensation in KB cells. Moreover, allicin concentration-dependently arrested KB cells at the S-phase of the cell cycle in the range of （16-48） μg/mL. In addition, treatment with the compound caused concentration-dependent disassembly of microtubule cytoskeleton in KB cells, which is similar to the effect of colchicine, a well-known microtubule destabilizing agent. We concluded that the abilities of allicin to inhibit the proliferation of KB cells probably relate to its apoptosis induction, cell cycle arrest and microtubule destabilizing properties.
