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. 2023 Oct 18;13:17803. doi: 10.1038/s41598-023-45017-2

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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/.

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CGA pretreatment reduces the expression levels of Lnc Neat1 and inhibits the activation of the NLRP3 inflammasome in HL-1 cardiomyocytes exposed to H/R. (a) HL-1 cardiomyocytes were pretreated with 0.2 μM CGA or 2 μM CGA for 12 h before H4R4. Effect of CGA on expression levels of Lnc Neat1 in HL-1 cardiomyocytes. The expression levels of Lnc Neat1 were measured by qRT-PCR. (b) Effect of CGA on mRNA expression levels of NLRP3 and ASC in HL-1 cardiomyocytes. The mRNA expression levels of NLRP3 and ASC were measured by qRT-PCR. (c,d) CGA pretreatment reduced the H/R injury-induced high protein expression levels of NLRP3 in HL-1 cardiomyocytes. The protein expression levels of NLRP3 were measuring by Western blotting analysis. (e) CGA pretreatment markedly inhibited H/R injury-mediated ASC oligomerization in HL-1 cardiomyocytes. ASC oligomerization was measuring by Western blotting analysis. The data are expressed as the mean ± SD. n = 3 independent experiments. The full-length blots are presented in Supplementary Fig. 2. *P < 0.05 vs. the control group, ^# P < 0.05 vs. the H4R4 group.