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. 2021 Mar 29;11:7117. doi: 10.1038/s41598-021-86514-6

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© The Author(s) 2021

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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Urolithin A controlled NF-kB inflammatory response. LPS stimulates TLR4 signalling cascades. Urolithin A impairs the NF-kB activation through the inactivation of IKKs. Urolithin A suppresses MAPKs activation through blocking ERK, p38 and JNK phosphorylation. Additionally, urolithin A inhibits the phosphorylation of AKT and mTOR protein. Abbreviation: LPS; lipopolysaccharide; IR, ionizing radiation; TIRAP, TIR adaptor protein; MyD88, myeloid differentiation primary-response gene 88; IRAK, interleukin-1 receptor associated kinase; TRAF, TNF receptor associated factor; RIP, receptor-interacting protein kinases; TAK, transforming growth factor beta-activated kinase 1; IKK, IκB kinase; MAPK, mitogen activated protein kinase; PI3K, phosphatidylinositol 3-kinases; mTOR, mechanistic target of rapamycin; ERK, extracellular regulated kinase; JNK, c-Jun N-terminal kinase; NF-κB, nuclear factor-κB; IκB, kinase complex; AP, activator protein; IL, interleukin; IFN, interferon; TNF, tumor necrosis factor; and NOS, nitric oxide.