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Fig. 4 | Journal of Nanobiotechnology

Fig. 4

From: Neuromodulation by nanozymes and ultrasound during Alzheimer’s disease management

Fig. 4

Different stimuli-responsive nanozymes. A Schematic Illustration of Biodegradation-Medicated Enzymatic Activity-Tunable Molybdenum Oxide Nanourchins (MoO3–x NUs) with the Highly Specific Toxicity to Tumor Tissues via a Multienzyme Stepwise Cascade Catalysis in Acidic Tumor Microenvironment, While Leaving Normal Tissues Unharmed Due to Their pH-Responsive Biodegradation and Subsequent Renal Excretion in Physiological Environment. Reproduced with permission [74]. copyright 2019, American Chemical Society. B Schematic illustration of piezoelectric dissociation of Alzheimer's β-amyloid (Aβ) aggregates on the surface of bismuth oxychloride (BiOCl) nanosheets. BiOCl nanosheet is a (001)-facet dominant piezoelectric material that possesses an anisotropic layered structure consisting of [Bi2O2]2+ slabs and interleaved double chloride anionic slabs along [001] direction. Under ultrasound stimulation, the change of local dipole moment in the BiOCl nanosheets induces piezoelectric polarization (Ppiezo) and separates electron–hole pairs by generating internal electric field (IEF). The separated charge carriers trigger piezocatalytic redox reactions of water and dissolved oxygen molecules. The produced reactive oxidative species, such as OH, O2, and H2O2, oxidize and dissociate the highly-stable, self-assembled Aβ aggregates (e.g., Aβ fibrils, plaques) into denatured fragments. Reproduced with permission [75]. copyright 2020, Elsevier. C, A Schematic illustration of the synthesis process for the versatile RGD-CCmMC/DOX nanovehicles and B schematic illustration of the therapeutic mechanism of the RGD-CCmMC/DOX nanoplatforms to enhance the overall anticancer efficiency of triple-combination photodynamic/photothermal/chemo-therapy in a solid tumor. Reproduced with permission [76]. copyright 2019, American Chemical Society. D Construction of self-sacrificing iron oxide nanoparticles with cisplatin (IV) prodrug (FePt-NP2) circumvents the endocytosis of cisplatin into the cells. In this way, excess OH are formed, which results in fast lipid and protein oxidation and DNA damage, as well as apoptosis via the ROS/Cyt C/caspase-3 pathway. Reproduced with permission [77]. copyright 2017, American Chemical Society

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