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Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway
PURPOSE: Inflammation is the driving force of many inflammatory and autoimmune diseases, Pyroptosis is a process of cell death in response to excessive inflammation. Punicalin has been reported to have anti-inflammatory effects. However, the anti-pyroptosis is unknown. Hence, this study was aimed to...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7943540/ https://www.ncbi.nlm.nih.gov/pubmed/33707964 http://dx.doi.org/10.2147/JIR.S299163 |
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author | Shen, Ruiting Yin, Peng Yao, Hua Chen, Lu Chang, Xinyu Li, Huanrong Hou, Xiaolin |
author_facet | Shen, Ruiting Yin, Peng Yao, Hua Chen, Lu Chang, Xinyu Li, Huanrong Hou, Xiaolin |
author_sort | Shen, Ruiting |
collection | PubMed |
description | PURPOSE: Inflammation is the driving force of many inflammatory and autoimmune diseases, Pyroptosis is a process of cell death in response to excessive inflammation. Punicalin has been reported to have anti-inflammatory effects. However, the anti-pyroptosis is unknown. Hence, this study was aimed to research the inhibition of MG on LPS/ATP-induced pyroptosis in vitro. METHODS: Lipopolysaccharide (LPS)/ATP were used to simulate mouse J774A.1 cells to mimic the inflammatory response and the role of punicalin was examined. The secretion of proinflammatory cytokines was analyzed using enzyme-linked immunosorbent assay (ELISA). The expression of nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC), caspase-1, and GSDMD-N in LPS/ATP-stimulated cells were examined by Western blot. N-acetylcysteine (NAC) was used to validate the role of Punicalin. RESULTS: Punicalin significantly blocked the production of endogenous ROS, reduced LPS/ATP-induced activation of NLRP3, caspase 1, ASC and GSDMD-N, IL-1b and IL-18 protein levels. Furthermore, N-acetylcysteine (NAC), an ROS scavenger, inhibited the LPS/ATP-stimulated activation of NLRP3 inflammasome mediated inflammation and pyroptosis. CONCLUSION: Punicalin ameliorates LPS/ATP-induced pyroptosis in J774A.1 macrophages, the mechanism may involve downregulation of the ROS/NLRP3 inflammasome signaling pathway. |
format | Online Article Text |
id | pubmed-7943540 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-79435402021-03-10 Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway Shen, Ruiting Yin, Peng Yao, Hua Chen, Lu Chang, Xinyu Li, Huanrong Hou, Xiaolin J Inflamm Res Original Research PURPOSE: Inflammation is the driving force of many inflammatory and autoimmune diseases, Pyroptosis is a process of cell death in response to excessive inflammation. Punicalin has been reported to have anti-inflammatory effects. However, the anti-pyroptosis is unknown. Hence, this study was aimed to research the inhibition of MG on LPS/ATP-induced pyroptosis in vitro. METHODS: Lipopolysaccharide (LPS)/ATP were used to simulate mouse J774A.1 cells to mimic the inflammatory response and the role of punicalin was examined. The secretion of proinflammatory cytokines was analyzed using enzyme-linked immunosorbent assay (ELISA). The expression of nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3), apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC), caspase-1, and GSDMD-N in LPS/ATP-stimulated cells were examined by Western blot. N-acetylcysteine (NAC) was used to validate the role of Punicalin. RESULTS: Punicalin significantly blocked the production of endogenous ROS, reduced LPS/ATP-induced activation of NLRP3, caspase 1, ASC and GSDMD-N, IL-1b and IL-18 protein levels. Furthermore, N-acetylcysteine (NAC), an ROS scavenger, inhibited the LPS/ATP-stimulated activation of NLRP3 inflammasome mediated inflammation and pyroptosis. CONCLUSION: Punicalin ameliorates LPS/ATP-induced pyroptosis in J774A.1 macrophages, the mechanism may involve downregulation of the ROS/NLRP3 inflammasome signaling pathway. Dove 2021-03-05 /pmc/articles/PMC7943540/ /pubmed/33707964 http://dx.doi.org/10.2147/JIR.S299163 Text en © 2021 Shen et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Shen, Ruiting Yin, Peng Yao, Hua Chen, Lu Chang, Xinyu Li, Huanrong Hou, Xiaolin Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway |
title | Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway |
title_full | Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway |
title_fullStr | Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway |
title_full_unstemmed | Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway |
title_short | Punicalin Ameliorates Cell Pyroptosis Induced by LPS/ATP Through Suppression of ROS/NLRP3 Pathway |
title_sort | punicalin ameliorates cell pyroptosis induced by lps/atp through suppression of ros/nlrp3 pathway |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7943540/ https://www.ncbi.nlm.nih.gov/pubmed/33707964 http://dx.doi.org/10.2147/JIR.S299163 |
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