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. 2022 Aug 23;31:09636897221077928. doi: 10.1177/09636897221077928

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© The Author(s) 2022

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 1. — NLRP3 is overexpressed in mice MI models and hypoxia-induced myocardial cells. (A) RT-qPCR and WB detected the NLRP3 level in infarct zone, border zone, and remote zone after MI for 4, 24, and 72 h, respectively. (B, C) RT-qPCR and WB measured IL-1β and IL-18 expression in infarct zone, border zone, and remote zone after MI for 4, 24, and 72 h, respectively. (D) The expression of NLRP3, IL-1β, and IL-18 was assessed in hypoxia HCMs compared with the normal group through RT-qPCR and WB. (E) The expression of NLRP3 was detected in hypoxia HCMs transfected with shRNAs targeting NLRP3 via RT-qPCR and WB. (F) RT-qPCR examined the expression of IL-1β and IL-18 after NLRP3 silencing in hypoxia HCMs. (G) RT-qPCR and WB evaluated NLRP3 level in normal HCMs transfected with pcDNA3.1/NLRP3. (H) The expression of IL-1β and IL-18 was examined in normal HCMs transfected with pcDNA3.1/NLRP3 using RT-qPCR. HCM: human cardiomyocytes; MI: myocardial infarction; NLRP3: NLR family pyrin domain containing 3; NLRP3: NLR family pyrin domain containing 3; RT-qPCR: reverse transcription quantitative polymerase chain rection; WB: western blot. **P < 0.01.