尽管还有改进的空间，联合疗法已成为治疗肿瘤的一种有前途的方法。这项研究引入了一种新策略，将细胞凋亡、铁死亡和 DNA 损伤的增强结合起来，以改善前列腺癌的治疗结果。具体来说，我们开发了一种超分子氧化应激纳米放大器，由β-环糊精、紫杉醇和二茂铁聚乙二醇组成。系统内的紫杉醇破坏微管动力学，诱导 G2/M 期停滞和细胞凋亡。同时，二茂铁利用过氧化氢通过芬顿反应在细胞中产生有毒的羟基自由基，引发一系列活性氧扩张、谷胱甘肽水平降低、脂质过氧化和铁死亡的级联。羟基自由基数量的增加以及 THZ531 对 DNA 修复机制的抑制作用加剧了肿瘤细胞内的 DNA 损伤。正如预期的那样，超分子纳米粒子对肿瘤细胞或组织表现出优异的药物递送能力，在体内表现出良好的生物安全性，并增强了对前列腺癌的杀伤作用。

Combination therapy has emerged as a promising approach for treating tumors, although there is room for improvement. This study introduced a novel strategy that combined the enhancement of apoptosis, ferroptosis, and DNA damage to improve therapeutic outcomes for prostate cancer. Specifically, we have developed a supramolecular oxidative stress nanoamplifier, which was comprised of β-cyclodextrin, paclitaxel, and ferrocene-poly(ethylene glycol). Paclitaxel within the system disrupted microtubule dynamics, inducing G2/M phase arrest and apoptosis. Concurrently, ferrocene utilized hydrogen peroxide to generate toxic hydroxyl radicals in cells through the Fenton reaction, triggering a cascade of reactive oxygen species expansion, reduction of glutathione levels, lipid peroxidation, and ferroptosis. The increased number of hydroxyl radicals and the inhibitory effect of THZ531 on DNA repair mechanisms exacerbated DNA damage within tumor cells. As expected, the supramolecular nanoparticles demonstrated excellent drug delivery ability to tumor cells or tissues, exhibited favorable biological safety in vivo, and enhanced the killing effect on prostate cancer.