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. 2023 Aug 22;21:286. doi: 10.1186/s12951-023-02013-y

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Mitochondrial damage-induced apoptosis of 4T1 cells by control, Blank NPs, DTX, DTX/CA-Oxi-αCD NPs and DTX/FA-CA-Oxi-αCD NPs, respectively. (A) CLSM images of JC-1 stained cells after different treatments. Scale bar represents 20 μm. (B) Western blot analysis for the expression of cleaved caspase-3 protein, phosphorylated Bcl-2 protein in 4T1 cells with different treatments for 48 h. (C) Quantitative analysis of cleaved caspase-3 protein expression in 4T1 cells. (D) Quantitative analysis of phosphorylated Bcl-2 protein expression in 4T1 cells. *p < 0.05, **p < 0.01, ***p < 0.001 compared with DTX/FA-CA-Oxi-αCD NPs (n = 3)