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. 2019 Jan 28;10(2):81. doi: 10.1038/s41419-018-1247-9

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© The Author(s) 2019

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — A schematic diagram represents the molecular mechanism of nimbolide in LPS-induced ARDS. The bacterial endotoxin, lipopolysaccharide (LPS) binds to its cognate toll-like receptor 4 (TLR-4) and the co-receptor cluster of differentiation 14 (CD14), which results in neutrophil accumulation, elevated vascular permeability, provocation of pulmonary edema. Nimbolide suppresses the nuclear translocation of NF-κB and HDAC-3. RNS- and ROS-induced ARDS is prevented by nimbolide by different canonical pathways

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