近來研究顯示大蒜具有防治腫瘤和癌癥的功效,。大蒜中的鍺和硒等元素可抑制腫瘤細(xì)胞和癌細(xì)胞的生長,，早期實(shí)驗(yàn)發(fā)現(xiàn),，癌癥發(fā)生率最低的人群就是血液中含硒量最高的人群。美國國家癌癥組織認(rèn)為,，全世界最具抗癌潛力的植物中，位居榜首的是大蒜,。
大蒜衍生的有機(jī)硫化合物（OSCS）包括硫化二烯丙基是眾所周知的具有多種健康益處的化合物,，最近的一項(xiàng)研究報(bào)告指出，由于其特有的選擇性的抗增殖作用,，在癌癥的化學(xué)預(yù)防和治療發(fā)面呈現(xiàn)了非常大的開發(fā)前景,。
研究報(bào)告指出硫化二烯丙基能阻斷早期有絲分裂，誘導(dǎo)細(xì)胞凋亡,。但潛在的分子機(jī)制尚未完全闡明,。研究數(shù)據(jù)顯示多硫化二烯丙基(類)化合物作用于活性氧（ROS）和微管蛋白。微管解聚防止正常主軸微管的形成,，從而導(dǎo)致G2/M停滯
研究數(shù)據(jù)表明多硫化二烯丙基(類)化合物可激活JNK,，介導(dǎo)抗凋亡蛋白Bcl-2的磷酸化和下游蛋白質(zhì)的表達(dá)，發(fā)揮抗腫瘤增殖功效,。（生物谷：Bioon.com）
doi:10.1093/carcin/bgs240
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Ros-Independent Jnk Activation and Multi-Site Phosphorylation of Bcl-2 Link Diallyl Tetrasulfide-Induced Mitotic Arrest to Apoptosis.
Kelkel M, Cerella C, Mack F, Schneider T, Jacob C, Schumacher M, Dicato M, Diederich M.
Garlic-derived organosulfur compounds (OSCs) including diallylpolysulfides are well known for various health-beneficial properties and recent reports even point to a potential role of diallylpolysulfides as chemopreventive and -therapeutic agents in cancer treatment due to their selective anti-proliferative effects. In this respect, diallyltri- and -tetrasulfide are reported as strong inducers of an early mitotic arrest and subsequent apoptosis, but the underlying molecular mechanisms and the link between these two events are not yet fully elucidated. Our data revealed that diallyltetrasulfide (DAS4) acts independently of reactive oxygen species (ROS) and tubulin represents one of its major cellular targets. Tubulin depolymerization prevents the formation of normal spindle microtubules thereby leading to G2/M arrest. Here, we provide evidence that JNK, which is activated early in response to DAS4 treatment, mediates multi-site phosphorylation and subsequent proteolysis of the anti-apoptotic protein Bcl-2. As the latter event occurs concomitantly with the onset of apoptosis and the chemical JNK inhibitor SP600125 not only prevented Bcl-2 phosphorylation and proteolysis but also apoptosis following DAS4 treatment, we suggest that these JNK-mediated modulations of Bcl-2 represent the missing link connecting early microtubule inactivation to the induction of apoptosis.
