山葵提取物诱导结肠癌细胞凋亡和自噬
The induction of apoptosis and autophagy by Wasabia japonica extract in colon cancer.
机构信息
Institute of Biochemistry and Biotechnology, Medical College, Chung Shan Medical University, Taichung, Taiwan.
Research Institute of Biotechnology, Hung Kuang University, Taichung, Taiwan.
出版信息
Eur J Nutr. 2016 Mar;55(2):491-503. doi: 10.1007/s00394-015-0866-5. Epub 2015 Feb 27.
PURPOSE
Wasabia japonica (wasabi) has been shown to exhibit properties of detoxification, anti-inflammation and the induction of apoptosis in cancer cells. This study aimed to investigate the molecular mechanism of the cytotoxicity of wasabi extract (WE) in colon cancer cells to evaluate the potential of wasabi as a functional food for chemoprevention.
METHODS
Colo 205 cells were treated with different doses of WE, and the cytotoxicity was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide. Apoptosis and autophagy were detected by 4',6-diamidino-2-phenylindole, 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethyl-imidacarbo-yanine iodide and staining for acidic vascular organelles (AVOs), along with Western blotting.
RESULTS
The results demonstrated that WE induced the extrinsic pathway and mitochondrial death machinery through the activation of TNF-α, Fas-L, caspases, truncated Bid and cytochrome C. WE also induced autophagy by decreasing the phosphorylation of Akt and mTOR and promoting the expression of microtubule-associated protein 1 light chain 3-II and AVO formation. An in vivo xenograft model verified that tumor growth was delayed by WE treatment.
CONCLUSION
Our studies revealed that WE exhibits anti-colon cancer properties through the induction of apoptosis and autophagy. These results provide support for the application of WE as a chemopreventive functional food and as a prospective treatment of colon cancer.
目的
青芥辣（wasabi）已被证明具有解毒、抗炎和诱导癌细胞凋亡的特性。本研究旨在探讨青芥辣提取物（WE）对结肠癌细胞的细胞毒性的分子机制，以评估青芥辣作为化学预防功能性食品的潜力。
方法
用不同剂量的 WE 处理 Colo 205 细胞，通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐分析细胞毒性。通过 4'，6-二脒基-2-苯基吲哚、5,5'，6,6'-四氯-1,1',3,3'-四乙基-碘化脒和酸性血管细胞器（AVOs）染色检测凋亡和自噬，并通过 Western blot 进行检测。
结果
结果表明，WE 通过激活 TNF-α、Fas-L、caspases、截断的 Bid 和细胞色素 C 诱导外源性途径和线粒体死亡机制。WE 通过降低 Akt 和 mTOR 的磷酸化以及促进微管相关蛋白 1 轻链 3-II 和 AVO 形成来诱导自噬。体内异种移植模型验证了 WE 治疗可延缓肿瘤生长。
结论
我们的研究表明，WE 通过诱导细胞凋亡和自噬来发挥抗结肠癌细胞的作用。这些结果为 WE 作为化学预防功能性食品的应用以及作为结肠癌的潜在治疗方法提供了支持。
Zotero 插件