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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 2. — Silencing of NLRP3 promotes proliferation and suppresses apoptosis of hypoxia-induced myocardial cells. (A) EdU assays testified the proliferation ability of hypoxia HCMs transfected with shRNAs targeting NLRP3 or of normal HCMs transfected with pcDNA3.1/NLRP3. (B, C) Flow cytometry and TUNEL assays examined the apoptosis rate of hypoxia HCMs transfected with shRNAs targeting NLRP3 or of normal HCMs transfected with pcDNA3.1/NLRP3. HCM: human cardiomyocytes; NLRP3: NLR family pyrin domain containing 3; shRNA: short hairpin RNA; DAPI: 4’,6-diamidino-2-phenylindole. **P < 0.01.