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. 2018 Nov 10;10(5):1401–1409. doi: 10.1039/c8sc04012e

Fig. 4. CL-driven photoisomerization for CPT release in in vitro antitumor effect. (a) Schematic illustration of positive-feedback-promoted H2O2 production mechanism and amplified isomerization mechanism of EAZO in cells. (b) Cytotoxicity of normal 3T3 cells as well as tumor 4T1, U-87 MG, and B16F10 cells after 24 h incubation with CLDRSs with different concentrations. ***P < 0.001. (c) Cell viability of normal 3T3 cells as well as tumor 4T1, U-87 MG, and B16F10 cells with various treatments (CLDRSs, 50 μg mL–1; equal 9.3 μg mL–1 of CPT). ***P < 0.001. (d) Schematic illustration of H2O2-suppressed mechanism in cells by adding GSH. Cells were incubated with CLDRSs. After 2 hours, the cells were washed twice with PBS and GSH (10 μM) added. (e) Cytotoxicity of CLDRSs (50 μg mL–1; equal 9.3 μg mL–1 of CPT) treatment with and without GSH. **P < 0.01. (f) Schematic illustration of the chemotherapy efficacy of CLDRSs compared with chemotherapy with external light irradiation. Cell viability of CPT@PEAZO-PCD NPs (equal 9.3 μg mL–1 of CPT) with different light dose (436 nm) in tumor (g) 4T1, (h) U-87 MG, and (i) B16F10 cells. ***P < 0.001. Error bars indicate the s.d. (n = 3).

Fig. 4