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...

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Autores principales: Li Haolan, Sun Aichen, Meng Taocheng, Zhu Yan
Formato: article
Lenguaje:EN
Publicado: De Gruyter 2020
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Acceso en línea:https://doaj.org/article/b398d5faa49f474a92e424c4e79939e2
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spelling oai:doaj.org-article:b398d5faa49f474a92e424c4e79939e22021-12-05T14:10:53ZExpression and role of ABIN1 in sepsis: In vitro and in vivo studies2391-546310.1515/med-2021-0008https://doaj.org/article/b398d5faa49f474a92e424c4e79939e22020-12-01T00:00:00Zhttps://doi.org/10.1515/med-2021-0008https://doaj.org/toc/2391-5463In 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.Li HaolanSun AichenMeng TaochengZhu YanDe Gruyterarticleabin1inflammationmacrophagessepsisMedicineRENOpen Medicine, Vol 16, Iss 1, Pp 033-040 (2020)
institution DOAJ
collection DOAJ
language EN
topic abin1
inflammation
macrophages
sepsis
Medicine
R
spellingShingle abin1
inflammation
macrophages
sepsis
Medicine
R
Li Haolan
Sun Aichen
Meng Taocheng
Zhu Yan
Expression and role of ABIN1 in sepsis: In vitro and in vivo studies
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 article
author Li Haolan
Sun Aichen
Meng Taocheng
Zhu Yan
author_facet Li Haolan
Sun Aichen
Meng Taocheng
Zhu Yan
author_sort Li Haolan
title 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_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_sort expression and role of abin1 in sepsis: in vitro and in vivo studies
publisher De Gruyter
publishDate 2020
url https://doaj.org/article/b398d5faa49f474a92e424c4e79939e2
work_keys_str_mv AT lihaolan expressionandroleofabin1insepsisinvitroandinvivostudies
AT sunaichen expressionandroleofabin1insepsisinvitroandinvivostudies
AT mengtaocheng expressionandroleofabin1insepsisinvitroandinvivostudies
AT zhuyan expressionandroleofabin1insepsisinvitroandinvivostudies
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