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. 2024 Feb 17;22:168. doi: 10.1186/s12967-024-04981-7

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© The Author(s) 2024

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. 6 — DSPE-PEG-CMP-miR302-EXO treatment significantly inhibited inflammatory response and IR injury. A–D ELISA showed that DSPE-PEG-CMP-miR302-EXO decreased levels of cTnI, CKMB, TNF-α and IL-1β in cardiomyocytes. A cTnI: cardiac troponin I; B CKMB: creatine kinase MB; C TNF-α: tumor necrosis factor-alpha; D IL-1β: interleukin (IL)-1 beta (β). E, F The miR302 level in serum and heart was detected with qRT-PCR, wherein the level was higher in DSPE-PEG-CMP-miR302-EXO group. Relative values were presented as fold change over control. G HE staining image showed reduced heart necrosis in the myocardial I/R injury after DSPE-PEG-CMP-miR302-EXO treatment. Scale bar = 100 μm