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. 2022 Jun 17;12:10275. doi: 10.1038/s41598-022-14491-5

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© The Author(s) 2022

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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NIN regulates cytokine-induced cytokine expression in CSMC. CSMC were stimulated with the pro-inflammatory cytokines IL-1β and TNFα (50 or 5 ng/mL each) and cytokine expression determined by qPCR at 6 or 48 h. (A) Increased expression of the pro-inflammatory cytokines IL-1β, TNFα, IL6 and IL8 but not IL17 or TGFβ at 6 and 48 h. Note large further increases in IL-1β and TNFα between 6 and 48 h. (B) Reduced level of stimulation IL-1β/TNFα (5 ng/mL each; 6 h exposure) maintains significant stimulation of IL-1β, TNFα, IL6 and IL8 but not IL17. (C) NIN (1 µM) reduces cytokine-induced expression of IL-1β and TNFα, but does not affect IL6, IL8 or IL17. Data expressed relative to cytokine-stimulated control (n = 4 cell lines), with stimulus of TNFα and IL-1β at 5 ng/mL for 6 h. Data, all p < 0.05 vs respective controls.