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Baicalin-Induced Autophagy Preserved LPS-Stimulated Intestinal Cells from Inflammation and Alterations of Paracellular Permeability

Several studies have demonstrated a relevant role of intestinal epithelial cells in the immune response and in chronic inflammatory conditions, including ulcers, colitis, and Crohn’s disease. Baicalin (BA), extracted from the root of Scutellaria baicalensis, has various beneficial healthy effects, i...

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Autores principales: Rizzo, Valentina, Ferlazzo, Nadia, Currò, Monica, Isola, Gaetano, Matarese, Marco, Bertuccio, Maria Paola, Caccamo, Daniela, Matarese, Giovanni, Ientile, Riccardo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7956379/
https://www.ncbi.nlm.nih.gov/pubmed/33652555
http://dx.doi.org/10.3390/ijms22052315
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author Rizzo, Valentina
Ferlazzo, Nadia
Currò, Monica
Isola, Gaetano
Matarese, Marco
Bertuccio, Maria Paola
Caccamo, Daniela
Matarese, Giovanni
Ientile, Riccardo
author_facet Rizzo, Valentina
Ferlazzo, Nadia
Currò, Monica
Isola, Gaetano
Matarese, Marco
Bertuccio, Maria Paola
Caccamo, Daniela
Matarese, Giovanni
Ientile, Riccardo
author_sort Rizzo, Valentina
collection PubMed
description Several studies have demonstrated a relevant role of intestinal epithelial cells in the immune response and in chronic inflammatory conditions, including ulcers, colitis, and Crohn’s disease. Baicalin (BA), extracted from the root of Scutellaria baicalensis, has various beneficial healthy effects, including anti-inflammatory activity. However, few studies have evaluated BA effects on autophagic signaling in epithelial cell response to inflammatory stimuli. To explore possible beneficial effects of BA, HT-29 cells were exposed to lipopolysaccharide (LPS), in presence or absence of BA, for 4 h. We evaluated mRNA levels of autophagy-related genes and cytokines, triggering inflammatory response. Furthermore, the expression of claudin 1, involved in the regulation of paracellular permeability was analyzed. BA treatment repressed LPS-induced expression of TNF-α and IL-1β. The down-regulation of autophagy-related genes induced by LPS was counteracted by cell pretreatment with BA. Under these conditions, BA reduced the NF-κB activation caused by LPS. Also, BA restored mRNA and protein levels of claudin 1, which were reduced by LPS. In conclusion, in intestinal epithelial cells BA regulates the NF-κB activation and modulates both autophagic and inflammatory processes, leading to an improvement of paracellular permeability. These results suggest that the anti-inflammatory effects of BA can be associated to the regulation of autophagic flux.
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spelling pubmed-79563792021-03-16 Baicalin-Induced Autophagy Preserved LPS-Stimulated Intestinal Cells from Inflammation and Alterations of Paracellular Permeability Rizzo, Valentina Ferlazzo, Nadia Currò, Monica Isola, Gaetano Matarese, Marco Bertuccio, Maria Paola Caccamo, Daniela Matarese, Giovanni Ientile, Riccardo Int J Mol Sci Article Several studies have demonstrated a relevant role of intestinal epithelial cells in the immune response and in chronic inflammatory conditions, including ulcers, colitis, and Crohn’s disease. Baicalin (BA), extracted from the root of Scutellaria baicalensis, has various beneficial healthy effects, including anti-inflammatory activity. However, few studies have evaluated BA effects on autophagic signaling in epithelial cell response to inflammatory stimuli. To explore possible beneficial effects of BA, HT-29 cells were exposed to lipopolysaccharide (LPS), in presence or absence of BA, for 4 h. We evaluated mRNA levels of autophagy-related genes and cytokines, triggering inflammatory response. Furthermore, the expression of claudin 1, involved in the regulation of paracellular permeability was analyzed. BA treatment repressed LPS-induced expression of TNF-α and IL-1β. The down-regulation of autophagy-related genes induced by LPS was counteracted by cell pretreatment with BA. Under these conditions, BA reduced the NF-κB activation caused by LPS. Also, BA restored mRNA and protein levels of claudin 1, which were reduced by LPS. In conclusion, in intestinal epithelial cells BA regulates the NF-κB activation and modulates both autophagic and inflammatory processes, leading to an improvement of paracellular permeability. These results suggest that the anti-inflammatory effects of BA can be associated to the regulation of autophagic flux. MDPI 2021-02-26 /pmc/articles/PMC7956379/ /pubmed/33652555 http://dx.doi.org/10.3390/ijms22052315 Text en © 2021 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/).
spellingShingle Article
Rizzo, Valentina
Ferlazzo, Nadia
Currò, Monica
Isola, Gaetano
Matarese, Marco
Bertuccio, Maria Paola
Caccamo, Daniela
Matarese, Giovanni
Ientile, Riccardo
Baicalin-Induced Autophagy Preserved LPS-Stimulated Intestinal Cells from Inflammation and Alterations of Paracellular Permeability
title Baicalin-Induced Autophagy Preserved LPS-Stimulated Intestinal Cells from Inflammation and Alterations of Paracellular Permeability
title_full Baicalin-Induced Autophagy Preserved LPS-Stimulated Intestinal Cells from Inflammation and Alterations of Paracellular Permeability
title_fullStr Baicalin-Induced Autophagy Preserved LPS-Stimulated Intestinal Cells from Inflammation and Alterations of Paracellular Permeability
title_full_unstemmed Baicalin-Induced Autophagy Preserved LPS-Stimulated Intestinal Cells from Inflammation and Alterations of Paracellular Permeability
title_short Baicalin-Induced Autophagy Preserved LPS-Stimulated Intestinal Cells from Inflammation and Alterations of Paracellular Permeability
title_sort baicalin-induced autophagy preserved lps-stimulated intestinal cells from inflammation and alterations of paracellular permeability
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7956379/
https://www.ncbi.nlm.nih.gov/pubmed/33652555
http://dx.doi.org/10.3390/ijms22052315
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