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. 2020 Nov 25;13(12):423. doi: 10.3390/ph13120423

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Schematic representation of ZOL-macrophage cross-talk mechanisms. ZOL-mediated activation of TLR4 in macrophages accounted for the overexpression of mature form of IL-1β leading to M1- polarization. Red arrows indicate the action of ZOL on TLR4 activation and Kdm6 proteins overexpression. (): gene transcription; (): increase; (H3K27Me3 ): reduced methylation; all the other arrows indicate the direction of the flow; IL-1β, interleukin-1β; Kdm6a, lysine demethylase 6 A; Kdm6b, lysine demethylase 6 B; NF-κB, nuclear factor-κB; NLRP3, NACHT, LRR, and PYD domains-containing protein 3; TLR4, Toll-Like Receptor 4. See text for explanation [51,53,54].

Inline graphic — Schematic representation of ZOL-macrophage cross-talk mechanisms. ZOL-mediated activation of TLR4 in macrophages accounted for the overexpression of mature form of IL-1β leading to M1- polarization. Red arrows indicate the action of ZOL on TLR4 activation and Kdm6 proteins overexpression. (): gene transcription; (): increase; (H3K27Me3 ): reduced methylation; all the other arrows indicate the direction of the flow; IL-1β, interleukin-1β; Kdm6a, lysine demethylase 6 A; Kdm6b, lysine demethylase 6 B; NF-κB, nuclear factor-κB; NLRP3, NACHT, LRR, and PYD domains-containing protein 3; TLR4, Toll-Like Receptor 4. See text for explanation [51,53,54].