introduction
Cancer is the second leading cause of death in humans worldwide. From a global perspective, nearly one in six deaths are caused by cancer. How to target the combination of photodynamic mechanics to treat cancer has been the direction that many researchers are committed to. Among them, the modified silica nanoparticles are used as a nanoreactor to enhance the acid response to the tumor microenvironment, and the cell organelle can be further targeted, and the clinical application value has been confirmed by the combination of PDT treatment of the tumor.
Summary of results
Recently, Professor Liu Zhuang and Professor Li Bin (co-communication author) of Suzhou University of China developed a multi-stage response intelligent nanoparticle system to improve the therapeutic effect of PDT by solving some problems in traditional PDT. Catalyzing catalase (CAT) and a water-soluble H2O2 decomposing enzyme in the inner cavity of the hollow silica nanoparticles, and doping it into the silica lattice structure together with Ce6 (a photosensitizer) Prepared by a simple "one-pot" reaction. The research results were published in the internationally renowned journal Nano Letters under the title "Smart nano-reactors for pH-responsive tumor homingmitochondria-targeting, andenhanced photodynamic-immunotherapy of cancer".
Graphic guide
Figure 1. Preparation and characterization of materials
(a) Preparation of CAT@S/Ce6-CTPP/DPEG;
(b) TEM image of CAT@S/Ce6-CTPP/DPEG;
(c) HAADF-STEM and elemental maps of CAT@S/Ce6-CTPP/DPEG;
(d) zeta potential values ​​of CAT@S/Ce6-CTPP/SPEG and CAT@S/Ce6-CTPP/DPEG at different pH values;
(e) A graph showing the change in oxygen production by BSA@S/Ce6-CTPP/DPEG and CAT@S/Ce6-CTPP/DPEG;
(f) a graph of the amount of oxygen produced by different concentrations of CAT@S/Ce6-CTPP/DPEG;
(g) A change in enzyme activity of free catalase and CAT@S/Ce6-CTPP/DPEG after incubation of proteinase K.
Figure 2. In vitro experiment of PDT
(a) Process schematic diagram of CAT@S/Ce6-CTPP/DPEG enhancing PDT action;
(b) Toxicity experiments of different concentrations of CAT@S/Ce6-CTPP/DPEG on 4T1;
(c) Toxicity experiments of BSA@S/Ce6-CTPP/DPEG and CAT@S/Ce6-CTPP/DPEG with different concentrations of Ce6 on 4T1;
(d) Confocal images of CAT@S/Ce6-CTPP/SPEG and CAT@S/Ce6-CTPP/DPEG at different pH values;
(e) Toxicity tests of 4T1 at different pH values ​​of CAT@S/Ce6-CTPP/SPEG and CAT@S/Ce6-CTPP/DPEG with different concentrations of Ce6;
(f) Confocal images of the positions of CAT@S/Ce6/DPEG and CAT@S/Ce6-CTPP/DPEG in cells at different time points;
(g) according to the Pearson correlation coefficient (Rr) statistics in (f);
(h) Toxicity experiments of CAT@S/Ce6/DPEG and CAT@S/Ce6-CTPP/DPEG with different concentrations of Ce6 on 4T1.
Figure 3. In vivo imaging and tumor oxidation modulation experiments
(a) Fluorescence imaging of mice in CAT@S/Ce6-CTPP/SPEG and CAT@S/Ce6-CTPP/DPEG;
(b) In vitro fluorescence imaging of normal organs and tumors;
(c) Quantitative images of in vitro fluorescence imaging of major organs and tumors;
(d) a confocal image of a mouse tumor slice;
(e) PA image of tumor oxygenation status of mouse 4T1 tumor;
(f) a quantified map of tumor oxygen saturation based on (e)PA imaging;
(g) Immunofluorescence staining of tumor sections of different treatment groups.
Figure 4. CAT@S/Ce6-CTPP/DPEG for PDT in vivo therapy
(a) Tumor growth curve after PDT treatment in the 4T1 model;
(b) mean tumor weight maps for different groups after treatment;
(c) Photographs of all tumors taken from different groups of mice after the end of the study;
(d) changes in body weight of mice in different groups at different times;
(e) Tumor sections of H&E and TUNEL staining.
Figure 5. Blocking immunotherapy with PDT and CAT@S/Ce6-CTPP/DPEG checkpoints
(a) combing the PDT and anti-PD-L1 treatment experimental design;
(b) a graph of tumor growth on the left side;
(c) Average tumor weight map on day 18 on the left;
(d) Percentage of CTL penetration at day 18 on the left;
(e) a tumor growth curve on the right;
(f) On the right side of the 18th day, the average tumor weight map;
(g) Percentage of CTL penetration at day 18 on the right;
(h) IFN-γ levels were detected from mouse serum 7 days after different treatments;
(i) a graph of changes in body weight during treatment;
(j) Schematic diagram of the mechanism of combination therapy of PDT and anti-PD-L1.
summary
Research and development of pH-responsive charge-switching, mitochondrial targeting and encapsulation of catalase-encapsulated hollow silica nanoparticles, and Ce6 doping as an intelligent nanoreactor for improving cancer PDT treatment. It makes the charge in the micro-acid environment of the tumor change from negative to positive, which is beneficial to cell internalization and tumor retention, enhances the targeting of mitochondria and the lethality of PDT to tumor cells, and simultaneously produces ROS. Some new strategies and methods are provided for the preparation of anti-tumor nanomaterials.
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