Abstract
Chemodynamic therapy as an emerging therapeutic strategy has been implemented for oncotherapy. However, the reactive oxygen species can be counteracted by the exorbitant glutathione (GSH) produced by the tumor cells before exerting the antitumor effect. Herein, borneol (NB) serving as a monoterpenoid sensitizer, and copper sulfide (CuS NPs) as an NIR-II photothermal agent were loaded in a thermo-responsive vehicle (NB/CuS@PCM NPs). Under 1,060-nm laser irradiation, the hyperthermia produced by CuS NPs can be used for photothermal therapy and melt the phase change material for drug delivery. In the acidity microenvironment, the CuS NPs released from NB/CuS@PCM NPs could degrade to Cu2+, then Cu2+ was reduced to Cu+ during the depletion of GSH. As Fenton-like catalyst, the copper ion could convert hydrogen peroxide into hydroxyl radicals for chemodynamic therapy. Moreover, the NB originated from NB/CuS@PCM NPs could increase the intracellular ROS content to improve the treatment outcome of chemodynamic therapy. The animal experimental results indicated that the NB/CuS@PCM NPs could accumulate at the tumor site and exhibit an excellent antitumor effect. This work confirmed that the combination of oxidative stress–induced damage and photothermal therapy is a potential therapeutic strategy for cancer treatment.
Highlights
Due to the hypoxic tumor microenvironment, tumor cells undergo hypoxic metabolism and inhabit in an elevated level of redox homeostasis circumstance (Yang et al, 2020)
NB, which serves as a chemosensitizer, can potentiate the therapeutic effect of anticancer drugs through cellular redox homeostasis interference by activating reactive oxygen species (ROS)-mediated oxidative damage (Horváthová et al, 2009; Su et al, 2013; Cao et al, 2020)
The absorbance spectrum of CuS NPs exhibited that gallic acid modified CuS NPs possess a strong NIR-II absorbance under different densities of 1,064-nm laser exposure
Summary
Due to the hypoxic tumor microenvironment, tumor cells undergo hypoxic metabolism and inhabit in an elevated level of redox homeostasis circumstance (Yang et al, 2020). Tumor cells will improve their antioxidant capacity, for example, the increased glutathione (GSH) levels in tumor cells further endow the tumor cells with anti-apoptosis and drug-resistant performance (Bansal and Simon, 2018; Liu Z. et al, 2020). The exorbitant GSH in tumor cells as a reactive oxygen species (ROS) scavenger dramatically reduces the therapeutic efficacy of ROS-medicated therapy and facilitates tumor metastasis, which makes cancer with high mortality and more difficult to be treated The overexpressed glutathione (GSH) in the malignant tumor generally attenuates the therapeutic effect of ROS-medicated therapy. The synergistic therapy with tumor microenvironment remodeling property is critical for the eradication of the malignant tumor (Liang et al, 2020)
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