Cargando…
Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6
Background. Under septic conditions, LPS induced lung vascular endothelial cell (EC) injury, and the release of inflammatory mediator launches and aggravates acute lung injury (ALI). There are no effective therapeutic options for ALI. Genistein-3′-sodium sulfonate (GSS) is a derivative of native soy...
Autores principales: | , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2019
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7012263/ https://www.ncbi.nlm.nih.gov/pubmed/32082076 http://dx.doi.org/10.1155/2019/4251394 |
_version_ | 1783496207858925568 |
---|---|
author | Yi, Lei Zhou, Zengding Zheng, Yijuan Chang, Mengling Huang, Xiaoqin Guo, Feng Zhao, Quanming Huan, Jingning |
author_facet | Yi, Lei Zhou, Zengding Zheng, Yijuan Chang, Mengling Huang, Xiaoqin Guo, Feng Zhao, Quanming Huan, Jingning |
author_sort | Yi, Lei |
collection | PubMed |
description | Background. Under septic conditions, LPS induced lung vascular endothelial cell (EC) injury, and the release of inflammatory mediator launches and aggravates acute lung injury (ALI). There are no effective therapeutic options for ALI. Genistein-3′-sodium sulfonate (GSS) is a derivative of native soy isoflavone, which exhibits neuroprotective effects via its antiapoptosis property. However, whether GSS protect against sepsis-induced EC injury and release of inflammatory mediators has not been determined. In this study, we found that GSS not only downregulated the levels of TNF-α and IL-6 in the lung and serum of mice in vivo but also inhibited the expression and secretion of TNF-α and IL-6 in ECs. Importantly, we also found that GSS blocked LPS-induced TNF-α and IL-6 expression in ECs via the Myd88/NF-κB signaling pathway. Taken together, our results demonstrated that GSS might be a promising candidate for sepsis-induced ALI via its regulating effects on inflammatory response in lung ECs. |
format | Online Article Text |
id | pubmed-7012263 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-70122632020-02-20 Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 Yi, Lei Zhou, Zengding Zheng, Yijuan Chang, Mengling Huang, Xiaoqin Guo, Feng Zhao, Quanming Huan, Jingning Mediators Inflamm Research Article Background. Under septic conditions, LPS induced lung vascular endothelial cell (EC) injury, and the release of inflammatory mediator launches and aggravates acute lung injury (ALI). There are no effective therapeutic options for ALI. Genistein-3′-sodium sulfonate (GSS) is a derivative of native soy isoflavone, which exhibits neuroprotective effects via its antiapoptosis property. However, whether GSS protect against sepsis-induced EC injury and release of inflammatory mediators has not been determined. In this study, we found that GSS not only downregulated the levels of TNF-α and IL-6 in the lung and serum of mice in vivo but also inhibited the expression and secretion of TNF-α and IL-6 in ECs. Importantly, we also found that GSS blocked LPS-induced TNF-α and IL-6 expression in ECs via the Myd88/NF-κB signaling pathway. Taken together, our results demonstrated that GSS might be a promising candidate for sepsis-induced ALI via its regulating effects on inflammatory response in lung ECs. Hindawi 2019-12-30 /pmc/articles/PMC7012263/ /pubmed/32082076 http://dx.doi.org/10.1155/2019/4251394 Text en Copyright © 2019 Lei Yi et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Yi, Lei Zhou, Zengding Zheng, Yijuan Chang, Mengling Huang, Xiaoqin Guo, Feng Zhao, Quanming Huan, Jingning Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
title | Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
title_full | Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
title_fullStr | Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
title_full_unstemmed | Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
title_short | Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
title_sort | suppressive effects of gss on lipopolysaccharide-induced endothelial cell injury and ali via tnf-α and il-6 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7012263/ https://www.ncbi.nlm.nih.gov/pubmed/32082076 http://dx.doi.org/10.1155/2019/4251394 |
work_keys_str_mv | AT yilei suppressiveeffectsofgssonlipopolysaccharideinducedendothelialcellinjuryandaliviatnfaandil6 AT zhouzengding suppressiveeffectsofgssonlipopolysaccharideinducedendothelialcellinjuryandaliviatnfaandil6 AT zhengyijuan suppressiveeffectsofgssonlipopolysaccharideinducedendothelialcellinjuryandaliviatnfaandil6 AT changmengling suppressiveeffectsofgssonlipopolysaccharideinducedendothelialcellinjuryandaliviatnfaandil6 AT huangxiaoqin suppressiveeffectsofgssonlipopolysaccharideinducedendothelialcellinjuryandaliviatnfaandil6 AT guofeng suppressiveeffectsofgssonlipopolysaccharideinducedendothelialcellinjuryandaliviatnfaandil6 AT zhaoquanming suppressiveeffectsofgssonlipopolysaccharideinducedendothelialcellinjuryandaliviatnfaandil6 AT huanjingning suppressiveeffectsofgssonlipopolysaccharideinducedendothelialcellinjuryandaliviatnfaandil6 |