Department of Biochemistry, University of Calcutta, 35, Ballygunge Circular Road, Kolkata 700019, India.
Materials Processing and Microsystems Laboratory, Central Mechanical Engineering Research Institute, Mahatma Gandhi Rd, Durgapur, West Bengal 713209, India.
Mater Sci Eng C Mater Biol Appl. 2019 Nov;104:109909. doi: 10.1016/j.msec.2019.109909. Epub 2019 Jun 22.
Redox-active quinones have been reported to show good potential for biological activities, while efforts are directed to explore the usefulness of these materials further in cancer management. Our previous study demonstrated that theaflavin and theaflavin-gallates (tea-extracted polyphenols) selectively induce apoptosis of tumour cells in vitro, but its concentration for showing half-maximal therapeutic response remains a matter of concern. In this report, we demonstrated that if theaflavin is conjugated with gold nanoparticles (AuNPs) to form a nanoconjugate AuNP@TfQ, its apoptotic ability increases significantly in comparison to the bare theaflavin (Tf). The nanoconjugate is prepared by following a one-step green synthesis ̶ a reaction between HAuCl and the aflavin at room temperature. AuNP@TfQ is characterized using particle size analysis, FESEM, UV-vis, FTIR, fluorescence, and X-ray photoelectron spectroscopytechniques. We assume that the enhanced anti-cancer effect of AuNP@TfQ appears due to the facile oxidation of the pristine theaflavin to its quinone derivative on the surface of AuNPs. The presence of quinone motif in AuNP@TfQ induces an increased level of ROS generation probably through the depolarization of mitochondria and resulted in the caspase-mediated apoptotic cell death which may hold the potential for a "magic bullet"-mediated ovarian cancer treatment.
氧化还原活性醌类化合物已被报道具有良好的生物活性潜力,而人们正在努力进一步探索这些材料在癌症管理中的有用性。我们之前的研究表明,茶黄素和茶黄素-没食子酸酯(茶叶中提取的多酚)在体外选择性诱导肿瘤细胞凋亡,但显示半最大治疗反应的浓度仍然是一个关注的问题。在本报告中,我们证明如果将茶黄素与金纳米粒子(AuNPs)结合形成纳米缀合物 AuNP@TfQ,其凋亡能力与裸露的茶黄素(Tf)相比显著增加。纳米缀合物是通过在室温下进行 HAuCl 和茶黄素之间的一步绿色合成反应制备的。使用粒径分析、FESEM、UV-vis、FTIR、荧光和 X 射线光电子能谱技术对 AuNP@TfQ 进行了表征。我们假设 AuNP@TfQ 的增强抗癌作用是由于 AuNPs 表面上原始茶黄素容易氧化为其醌衍生物。AuNP@TfQ 中醌基的存在可能通过线粒体去极化诱导 ROS 生成水平增加,导致 caspase 介导的凋亡细胞死亡,这可能为“魔弹”介导的卵巢癌治疗提供潜力。