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. 2023 Apr 21;13:6528. doi: 10.1038/s41598-023-33848-y

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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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HIF-1α is involved in the activation of NLRP3 inflammasome in irinotecan (IR)-treated HepG2 cells. (A) Echinomycin (Ech) treatment suppresses NLRP3 inflammasome activity in IR-treated HepG2 cells. Western blot analysis of NLRP3, cleaved-Caspase1 and IL-1β protein levels in HepG2 cells. (B) Densitometric quantification of NLRP3, cleaved-Caspase1 and IL-1β. (C) Ech treatment alleviates ROS production in IR-treated HepG2 cells. Relative ROS level in each group. (D) Effects of ROS production on HIF-1α and NLRP3 inflammasome activity in IR-treated HepG2 cells. Western blot analysis of HIF-1α, NLRP3, cleaved-Caspase1 and IL-1β protein levels in HepG2 cells. (E) Densitometric quantification of HIF-1α, NLRP3, cleaved-Caspase1 and IL-1β. The blots were cut prior to hybridization with indicated primary antibodies. Data are presented as mean ± SD (n = 3), *P < 0.05 and **P < 0.01 compared with normal control group, ^#P < 0.05 and ^##P < 0.01 compared with 20 μM IR-treated group.