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Vaspin Alleviates Sepsis-Induced Cardiac Injury and Cardiac Inflammation by Inhibiting Kallikrein 7 in Mice
BACKGROUND: Vaspin is an important adipokine that is involved in cardiovascular diseases. This study is aimed at investigating whether vaspin participates in sepsis-induced cardiac injury and explored the possible mechanism. METHODS: First, cecal ligation and puncture (CLP) and lipopolysaccharide (L...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9307398/ https://www.ncbi.nlm.nih.gov/pubmed/35873711 http://dx.doi.org/10.1155/2022/1149582 |
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author | Yin, Na Pan, Fuze Qiu, Lingyue Yang, Zicong Xiong, Rixin Shi, Lei Shi, Ying Wu, Ning Wu, Kui Li, Qingkuan Wen, Daojun Huang, Qili Zhang, Yuyan Mi, Yuhong Ji, Qingwei |
author_facet | Yin, Na Pan, Fuze Qiu, Lingyue Yang, Zicong Xiong, Rixin Shi, Lei Shi, Ying Wu, Ning Wu, Kui Li, Qingkuan Wen, Daojun Huang, Qili Zhang, Yuyan Mi, Yuhong Ji, Qingwei |
author_sort | Yin, Na |
collection | PubMed |
description | BACKGROUND: Vaspin is an important adipokine that is involved in cardiovascular diseases. This study is aimed at investigating whether vaspin participates in sepsis-induced cardiac injury and explored the possible mechanism. METHODS: First, cecal ligation and puncture (CLP) and lipopolysaccharide (LPS) were used to establish a mouse model of sepsis, and cardiac vaspin expression was examined. In addition, after pretreatment with vaspin or phosphate-buffered saline (PBS), wild-type (WT) mice underwent CLP to establish a septic model and received sham as a control. Finally, WT mice and kallikrein 7 (KLK7-/-) mice were underwent CLP with or without vaspin pretreatment. RESULTS: Mice that underwent CLP and were administered LPS exhibited increased vaspin expression in both the heart and serum compared with sham- or saline-treated mice. In CLP mice, pretreatment with vaspin reduced mortality and alleviated the expression of cardiac injury markers and cardiac dysfunction. In addition, vaspin reduced the cardiac levels of CD45+ cells and CD68+ cells, alleviated the cardiac inflammatory response, and reduced cardiomyocyte apoptosis. The protective effects of vaspin on CLP mice were masked by the deletion of KLK7, which was demonstrated to be a downstream signal of vaspin. CONCLUSIONS: Vaspin alleviates cardiac inflammation and plays a protective role in sepsis-induced cardiac injury by reducing KLK7 expression. |
format | Online Article Text |
id | pubmed-9307398 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-93073982022-07-23 Vaspin Alleviates Sepsis-Induced Cardiac Injury and Cardiac Inflammation by Inhibiting Kallikrein 7 in Mice Yin, Na Pan, Fuze Qiu, Lingyue Yang, Zicong Xiong, Rixin Shi, Lei Shi, Ying Wu, Ning Wu, Kui Li, Qingkuan Wen, Daojun Huang, Qili Zhang, Yuyan Mi, Yuhong Ji, Qingwei Mediators Inflamm Research Article BACKGROUND: Vaspin is an important adipokine that is involved in cardiovascular diseases. This study is aimed at investigating whether vaspin participates in sepsis-induced cardiac injury and explored the possible mechanism. METHODS: First, cecal ligation and puncture (CLP) and lipopolysaccharide (LPS) were used to establish a mouse model of sepsis, and cardiac vaspin expression was examined. In addition, after pretreatment with vaspin or phosphate-buffered saline (PBS), wild-type (WT) mice underwent CLP to establish a septic model and received sham as a control. Finally, WT mice and kallikrein 7 (KLK7-/-) mice were underwent CLP with or without vaspin pretreatment. RESULTS: Mice that underwent CLP and were administered LPS exhibited increased vaspin expression in both the heart and serum compared with sham- or saline-treated mice. In CLP mice, pretreatment with vaspin reduced mortality and alleviated the expression of cardiac injury markers and cardiac dysfunction. In addition, vaspin reduced the cardiac levels of CD45+ cells and CD68+ cells, alleviated the cardiac inflammatory response, and reduced cardiomyocyte apoptosis. The protective effects of vaspin on CLP mice were masked by the deletion of KLK7, which was demonstrated to be a downstream signal of vaspin. CONCLUSIONS: Vaspin alleviates cardiac inflammation and plays a protective role in sepsis-induced cardiac injury by reducing KLK7 expression. Hindawi 2022-07-15 /pmc/articles/PMC9307398/ /pubmed/35873711 http://dx.doi.org/10.1155/2022/1149582 Text en Copyright © 2022 Na Yin et al. https://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 Yin, Na Pan, Fuze Qiu, Lingyue Yang, Zicong Xiong, Rixin Shi, Lei Shi, Ying Wu, Ning Wu, Kui Li, Qingkuan Wen, Daojun Huang, Qili Zhang, Yuyan Mi, Yuhong Ji, Qingwei Vaspin Alleviates Sepsis-Induced Cardiac Injury and Cardiac Inflammation by Inhibiting Kallikrein 7 in Mice |
title | Vaspin Alleviates Sepsis-Induced Cardiac Injury and Cardiac Inflammation by Inhibiting Kallikrein 7 in Mice |
title_full | Vaspin Alleviates Sepsis-Induced Cardiac Injury and Cardiac Inflammation by Inhibiting Kallikrein 7 in Mice |
title_fullStr | Vaspin Alleviates Sepsis-Induced Cardiac Injury and Cardiac Inflammation by Inhibiting Kallikrein 7 in Mice |
title_full_unstemmed | Vaspin Alleviates Sepsis-Induced Cardiac Injury and Cardiac Inflammation by Inhibiting Kallikrein 7 in Mice |
title_short | Vaspin Alleviates Sepsis-Induced Cardiac Injury and Cardiac Inflammation by Inhibiting Kallikrein 7 in Mice |
title_sort | vaspin alleviates sepsis-induced cardiac injury and cardiac inflammation by inhibiting kallikrein 7 in mice |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9307398/ https://www.ncbi.nlm.nih.gov/pubmed/35873711 http://dx.doi.org/10.1155/2022/1149582 |
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