咖喱是多種香料的混合物,。它之所以具有殺死癌細胞的作用,，主要歸功于其配料中黃姜所含的姜黃素,。大多數(shù)情況下,，令癌細胞死亡的方法是通過激活細胞中的半胱氨酸蛋白酶（又稱凋亡蛋白酶），從而啟動癌細胞自身程序性凋亡,。
愛爾蘭科克癌癥研究中心研究員杰拉爾丁·奧沙利文科因和他的研究小組在試驗中發(fā)現(xiàn),，經(jīng)過姜黃素處理的癌細胞在24小時內(nèi)開始死亡，而其中半胱氨酸蛋白酶水平并沒有提高,。不僅如此,，研究人員即使使用其他藥物阻止半胱氨酸蛋白酶啟動程序性凋亡，癌細胞還是會死亡,。這說明姜黃素可以通過另一種全新途徑殺死癌細胞,。
科學家并非近期才意識到姜黃素具有醫(yī)學價值。這項研究的另一名負責人莎倫·麥克納說：“醫(yī)學界早已意識到某些天然物質(zhì)對治療癌癥具有潛在價值,，并且認為姜黃素可能就是其中一種。”先前曾有研究稱姜黃素對癌細胞有抑制作用，并指出常吃咖喱的人不易患癌癥,?？上М斂о蝗梭w消化吸收后，這種抗癌特性也就很快消失,。2007年美國科學家發(fā)現(xiàn),，姜黃素有助老年癡呆癥患者提高免疫力。還有人嘗試用姜黃素治療關(guān)節(jié)炎,。麥克納說,，姜黃素利用一種未知的“細胞語言”向癌細胞發(fā)出“死亡信號”。他們的研究表明可以直接從咖喱中提取姜黃素來研發(fā)治療癌癥的新藥,。（生物谷Bioon.com）
相關(guān)信息：
細胞凋亡分子機制
細胞凋亡與腫瘤
細胞凋亡研究：
Cell：細胞壞死狀凋亡分子機制
Nature Cell Biology：動植物的細胞凋亡方式相同
Science：RIP3具有細胞凋亡/細胞壞死開關(guān)作用
更多：細胞凋亡專題
細胞凋亡試劑大全
細胞凋亡檢測技術(shù)與方法
姜黃與癌癥：
咖喱粉中姜黃色素可抑制癌細胞生長
JBC：咖喱--對抗早老性癡呆的新武器
Janus激酶細胞信號轉(zhuǎn)導(dǎo)及轉(zhuǎn)錄活化因子通路抑制劑的研究進展
生物谷推薦原始出處：
British Journal of Cancer (2009) 101, 1585–1595. doi:10.1038/sj.bjc.6605308
Curcumin induces apoptosis-independent death in oesophageal cancer cells
G O'Sullivan-Coyne1, G C O'Sullivan1, T R O'Donovan1, K Piwocka2 and S L McKenna1
1Leslie C. Quick Laboratory, Cork Cancer Research Centre, BioSciences Institute, University College Cork and Mercy University Hospital, Cork, Ireland
2Nencki Institute of Experimental Biology, Warsaw, Poland
background: Oesophageal cancer incidence is increasing and survival rates remain extremely poor. Natural agents with potential for chemoprevention include the phytochemical curcumin (diferuloylmethane). We have examined the effects of curcumin on a panel of oesophageal cancer cell lines.
methods: MTT (3-(4,5-dimethyldiazol-2-yl)-2,5 diphenyl tetrazolium bromide) assays and propidium iodide staining were used to assess viability and DNA content, respectively. Mitotic catastrophe (MC), apoptosis and autophagy were defined by both morphological criteria and markers such as MPM-2, caspase 3 cleavage and monodansylcadaverine (MDC) staining. Cyclin B and poly-ubiquitinated proteins were assessed by western blotting.
results: Curcumin treatment reduces viability of all cell lines within 24 h of treatment in a 5–50 m range. Cytotoxicity is associated with accumulation in G2/M cell-cycle phases and distinct chromatin morphology, consistent with MC. Caspase-3 activation was detected in two out of four cell lines, but was a minor event. The addition of a caspase inhibitor zVAD had a marginal or no effect on cell viability, indicating predominance of a non-apoptotic form of cell death. In two cell lines, features of both MC and autophagy were apparent. Curcumin-responsive cells were found to accumulate poly-ubiquitinated proteins and cyclin B, consistent with a disturbance of the ubiquitin–proteasome system. This effect on a key cell-cycle checkpoint regulator may be responsible for the mitotic disturbances and consequent cytotoxicity of this drug.
conclusion: Curcumin can induce cell death by a mechanism that is not reliant on apoptosis induction, and thus represents a promising anticancer agent for prevention and treatment of oesophageal cancer.
