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. 2021 Sep 16;12(10):852. doi: 10.1038/s41419-021-04143-3

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© The Author(s) 2021

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — A Schematic diagram of the VX-765 treatment of AMI model. B Caspase1 activity is significantly decreased at 72 h AMI samples with VX-765 treatment (n = 3, ***P < 0.001, Student’s t test). C VX-765 treatment decreases the protein level of ACT-CASP1 not PRO-CASP1. Left: Western blotting analysis of pro-CASPASE1 and active-CASPASE1. Right: Quantification of pro-CASPASE1 and active-CASPASE1 of the Western blotting results (n = 3, **P < 0.01, Student’s t test). D Echocardiography results show the rescue effect of VX-765 treatment on AMI (n = 3, *P < 0.05, Student’s t test). E VX-765 treatment decreases the infarction region. Left: Masson staining results show the reduced size of the infarction region with VX-765 treatment. Arrows indicate the infarction region (blue). Right: quantification of the infarction region indicates VX-765 treatment significantly reduces the infarction region (n = 3, *P < 0.05, Student’s t test).