2023
DOI: 10.1016/j.nantod.2023.101759
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Inhibiting COX-2/PGE2 pathway with biodegradable NIR-Ⅱ fluorescent polymeric nanoparticles for enhanced photodynamic immunotherapy

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Cited by 13 publications
(5 citation statements)
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“…Moreover, tumor necrosis factor-𝛼 (TNF-𝛼) is a cytokine that can directly kill tumor cells without consequential toxicity to normal cells, and its increase can remarkably amplify the anti-tumor effect. [26] As expected, TNF-𝛼 was crucially increased in the tumor sections after synergistic therapy. The above results show that BSM has respectable biocompatibility and biosafety, can be applied to in vivo treatment, and its sono/photo-activated performance and promoted ICD powerfully reinforce the synergistic therapeutic effect.…”
Section: In Vivo Synergistic Therapysupporting
confidence: 66%
“…Moreover, tumor necrosis factor-𝛼 (TNF-𝛼) is a cytokine that can directly kill tumor cells without consequential toxicity to normal cells, and its increase can remarkably amplify the anti-tumor effect. [26] As expected, TNF-𝛼 was crucially increased in the tumor sections after synergistic therapy. The above results show that BSM has respectable biocompatibility and biosafety, can be applied to in vivo treatment, and its sono/photo-activated performance and promoted ICD powerfully reinforce the synergistic therapeutic effect.…”
Section: In Vivo Synergistic Therapysupporting
confidence: 66%
“…To this end, we designed a novel bis‐hydroxyl group containing BODIPY photosensitizer with a larger conjugated system, named MonoBodipy ( Figure A). [ 20 ] However, due to the extremely poor water solubility of MonoBodipy, it is difficult to directly apply it in vivo. In order to overcome this drawback, a polycondensation reaction was carried out by using the bis‐hydroxyl group containing MonoBodipy, a ROS‐sensitive monomer (2,2′‐(propane‐2,2‐diylbis(sulfanediyl))bis(ethan‐1‐ol), DSB) (Figure S1, Supporting Information) with two hydroxyl groups and 1,2,4,5‐cyclohexanetetracarboxylic dianhydride (HPMDA) at a molar feed ratio of 2:18:21.…”
Section: Resultsmentioning
confidence: 99%
“…Inhibiting the COX-2/PGE 2 pathway can downregulate PD-L1 expression [25] and improve the immunosuppressive TME. [20,24] As a nonsteroidal anti-inflammatory drug, DA effectively inhibits COX-2 expression and PGE 2 release. [46] To confirm the in vitro effects of CCP@DA on COX-2/PEG 2 and PD-L1 (Figure 2A), we analyzed COX-2 expression in mouse breast cancer cells (4T1 cells) using western blotting (WB) assay and confocal laser scanning microscope (CLSM) (Figure 2B-D).…”
Section: In Vitro Cox-2 and Peg 2 Inhibitionmentioning
confidence: 99%
“…However, the released pro-tumor inflammatory factors such as interleukin-6 (IL-6), tumor necrosis factor-𝛼 (TNF-𝛼), [19][20][21] the upregulated cycoperoxidase-2 (COX-2), and COX-2 mediating prostaglandin E2 (PGE 2 ) [22,23] also cause detrimental inflammatory responses. [24,25] The resulting inflammatory microenvironment blocks dendritic cells (DCs) migration, [26,27] activates programmed death ligand 1 (PD-L1) upregulation, [28,29] and recruits immunosuppressive cells [30][31][32] to promote an immunosuppressive microenvironment. [33] Suppressing phototherapy-induced detrimental inflammation while maintaining an immune-promoting inflammatory response is a Scheme 1.…”
Section: Introductionmentioning
confidence: 99%
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