Abstract：
Nanozyme activity is greatly weakened by the microenvironment and multidrug resistance of tumor cells. Hence, a bi-catalytic nanoplatform, which promotes the anti-tumor activity through \"charging empowerment\" and \"mutual complementation\" processes involved in enzymatic and pyroelectric catalysis, by loading ultra-small nanoparticles (USNPs) of pyroelectric ZnSnO3 onto MXene nanozyme (V2CTx nanosheets), is developed. Here, the V2CTx nanosheets exhibit enhanced peroxidase activity by reacting V3+ with H2O2 to generate toxic ·OH, accelerated by the near-infrared (NIR) light mediated heat effect. The resulting V4+ is then converted to V3+ by oxidizing endogenous glutathione (GSH), realizing an enzyme-catalyzed cycle. However, the cycle will lose its persistence once GSH is insufficient; nevertheless, the pyroelectric charges generated by ZnSnO3 USNPs continuously support the V4+/V3+ conversion and ensure nanoenzyme durability. Moreover, the hyperthermia arising from the V2CTx nanosheets by NIR irradiation results in an ideal local temperature gradient for the ZnSnO3 USNPs, giving rise to an excellent pyroelectric catalytic effect by promoting band bending. Furthermore, polarized charges increase the tumor cell membrane permeability and facilitate nanodrug accumulation, thereby resolving the multidrug resistance issue. Thus, the combination of pyroelectric and enzyme catalysis together with the photothermal effect solves the dilemma of nanozymes and improves the antitumor efficiency.
摘要：
纳米酶的活性被肿瘤细胞的微环境和多药耐药性大大削弱。因此，双催化纳米平台,通过参与酶和热电催化的“充电授权”和“相互互补”过程促进抗肿瘤活性，通过将热电ZnSnO3的超小纳米颗粒（USNP）加载到MXene纳米酶（V2CTx纳米片）上，已开发。这里,V2CTx纳米片通过V3+与H2O2反应产生毒性·OH而表现出增强的过氧化物酶活性，由近红外（NIR）光介导的热效应加速。然后通过氧化内源性谷胱甘肽（GSH）将所得的V4转化为V3，实现酶催化循环。然而,一旦GSH不足，循环将失去持久性；然而，由ZnSnO3USNPs产生的热电电荷持续支持V4+/V3+转化并确保纳米酶的耐久性。此外，由NIR照射的V2CTx纳米片引起的高温导致ZnSnO3USNP的理想局部温度梯度，通过促进带弯曲产生优异的热释电催化效果。此外，极化电荷增加肿瘤细胞膜的通透性，促进纳米药物的积累，从而解决多药耐药问题。因此，热释电和酶催化的结合以及光热效应解决了纳米酶的困境，提高了抗肿瘤效率。
