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Expression and role of ABIN1 in sepsis: In vitro and in vivo studies
In this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264.7 macrophages. LPS was adopted to treat RAW264.7 macrophages for 4 h, and the levels of inflammatory factors were assessed by ELISA. Besides, A...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
De Gruyter
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7729633/ https://www.ncbi.nlm.nih.gov/pubmed/33364432 http://dx.doi.org/10.1515/med-2021-0008 |
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author | Li, Haolan Sun, Aichen Meng, Taocheng Zhu, Yan |
author_facet | Li, Haolan Sun, Aichen Meng, Taocheng Zhu, Yan |
author_sort | Li, Haolan |
collection | PubMed |
description | In this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264.7 macrophages. LPS was adopted to treat RAW264.7 macrophages for 4 h, and the levels of inflammatory factors were assessed by ELISA. Besides, ABIN1 expression was measured by quantitative reverse transcription polymerase chain reaction. Apparently, LPS enhanced immunoreaction, suggested by increased expression of IL-1β, tumor necrosis factor (TNF)-α, and IL-6. ABIN1 levels were obviously reduced compared to the control. Furthermore, we evaluated the roles of ABIN1-plasmid in immunoreaction and nuclear factor-κB (NF-κB) pathway. We found that ABIN1-plasmid significantly reduced the expression of IL-1β, TNF-α, and IL-6 in LPS-treated cells and inhibited NF-κB pathway activation. Meanwhile, a septic mouse mode was conducted to validate the role of ABIN1 in inflammatory response and organ damage in vivo. These data suggested that ABIN1-plasmid significantly inhibited the secretion of inflammatory cytokines and Cr, BUN, AST, and ALT levels in the serum of LPS-stimulated mice compared to LPS + control-plasmid group, reflecting the relieved inflammation and organ injury. In summary, the present findings indicated that ABIN1 alleviated sepsis by repressing inflammatory response through NF-κB signaling pathway, emphasizing the potential value of ABIN1 as therapeutic strategy for sepsis. |
format | Online Article Text |
id | pubmed-7729633 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | De Gruyter |
record_format | MEDLINE/PubMed |
spelling | pubmed-77296332020-12-23 Expression and role of ABIN1 in sepsis: In vitro and in vivo studies Li, Haolan Sun, Aichen Meng, Taocheng Zhu, Yan Open Med (Wars) Research Article In this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264.7 macrophages. LPS was adopted to treat RAW264.7 macrophages for 4 h, and the levels of inflammatory factors were assessed by ELISA. Besides, ABIN1 expression was measured by quantitative reverse transcription polymerase chain reaction. Apparently, LPS enhanced immunoreaction, suggested by increased expression of IL-1β, tumor necrosis factor (TNF)-α, and IL-6. ABIN1 levels were obviously reduced compared to the control. Furthermore, we evaluated the roles of ABIN1-plasmid in immunoreaction and nuclear factor-κB (NF-κB) pathway. We found that ABIN1-plasmid significantly reduced the expression of IL-1β, TNF-α, and IL-6 in LPS-treated cells and inhibited NF-κB pathway activation. Meanwhile, a septic mouse mode was conducted to validate the role of ABIN1 in inflammatory response and organ damage in vivo. These data suggested that ABIN1-plasmid significantly inhibited the secretion of inflammatory cytokines and Cr, BUN, AST, and ALT levels in the serum of LPS-stimulated mice compared to LPS + control-plasmid group, reflecting the relieved inflammation and organ injury. In summary, the present findings indicated that ABIN1 alleviated sepsis by repressing inflammatory response through NF-κB signaling pathway, emphasizing the potential value of ABIN1 as therapeutic strategy for sepsis. De Gruyter 2020-12-04 /pmc/articles/PMC7729633/ /pubmed/33364432 http://dx.doi.org/10.1515/med-2021-0008 Text en © 2021 Haolan Li et al., published by De Gruyter http://creativecommons.org/licenses/by/4.0 This work is licensed under the Creative Commons Attribution 4.0 International License. |
spellingShingle | Research Article Li, Haolan Sun, Aichen Meng, Taocheng Zhu, Yan Expression and role of ABIN1 in sepsis: In vitro and in vivo studies |
title | Expression and role of ABIN1 in sepsis: In vitro and in vivo studies |
title_full | Expression and role of ABIN1 in sepsis: In vitro and in vivo studies |
title_fullStr | Expression and role of ABIN1 in sepsis: In vitro and in vivo studies |
title_full_unstemmed | Expression and role of ABIN1 in sepsis: In vitro and in vivo studies |
title_short | Expression and role of ABIN1 in sepsis: In vitro and in vivo studies |
title_sort | expression and role of abin1 in sepsis: in vitro and in vivo studies |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7729633/ https://www.ncbi.nlm.nih.gov/pubmed/33364432 http://dx.doi.org/10.1515/med-2021-0008 |
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