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Paeonol alleviates lipopolysaccharide-induced hepatocytes injury through alteration of mitochondrial function and NF-κB translocation

Sepsis is a severe disease, with high mortality. Permanent organ damage caused by sepsis reduces the quality of life of surviving patients. The liver is an easily damaged organ in sepsis and sepsis-associated liver injury foretells a poor prognosis. Unfortunately, there are no effective treatments o...

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Autores principales: Xu, Shouzhu, Xu, Jie, Hao, Ting, Yan, Yu, Zhang, Shihao, Li, Aihong, Shi, Chuandao, Liu, Qiling, Zhao, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8436227/
https://www.ncbi.nlm.nih.gov/pubmed/34498704
http://dx.doi.org/10.3892/mmr.2021.12419
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author Xu, Shouzhu
Xu, Jie
Hao, Ting
Yan, Yu
Zhang, Shihao
Li, Aihong
Shi, Chuandao
Liu, Qiling
Zhao, Jing
author_facet Xu, Shouzhu
Xu, Jie
Hao, Ting
Yan, Yu
Zhang, Shihao
Li, Aihong
Shi, Chuandao
Liu, Qiling
Zhao, Jing
author_sort Xu, Shouzhu
collection PubMed
description Sepsis is a severe disease, with high mortality. Permanent organ damage caused by sepsis reduces the quality of life of surviving patients. The liver is an easily damaged organ in sepsis and sepsis-associated liver injury foretells a poor prognosis. Unfortunately, there are no effective treatments or drugs to solve this problem. Therefore, strategies or novel drugs are urgently required to protect against liver dysfunction in sepsis. In the present study, lipopolysaccharide (LPS) was used to establish a model of liver injury in vitro. The data demonstrated that pretreatment of L02 human normal hepatocytes with paeonol (PAE) alleviated LPS-induced cell injury and decreased the levels of alanine aminotransferase and aspartate transaminase, indicating a protective effect of PAE. Further experiments demonstrated that PAE increased LPS-decreased L02 cell viability, the levels of superoxide dismutase and Bcl-2 expression. PAE decreased LPS-increased cell apoptosis, intracellular reactive oxygen species and the expression levels of Bax and cleaved-caspase-3. PAE decreased LPS-promoted mitochondrial depolarization and nuclear translocation of NF-κB. In conclusion, PAE alleviated LPS-induced liver injury via alteration of mitochondrial function and NF-κB translocation. Therefore, PAE has potential for the treatment of sepsis.
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spelling pubmed-84362272021-09-17 Paeonol alleviates lipopolysaccharide-induced hepatocytes injury through alteration of mitochondrial function and NF-κB translocation Xu, Shouzhu Xu, Jie Hao, Ting Yan, Yu Zhang, Shihao Li, Aihong Shi, Chuandao Liu, Qiling Zhao, Jing Mol Med Rep Articles Sepsis is a severe disease, with high mortality. Permanent organ damage caused by sepsis reduces the quality of life of surviving patients. The liver is an easily damaged organ in sepsis and sepsis-associated liver injury foretells a poor prognosis. Unfortunately, there are no effective treatments or drugs to solve this problem. Therefore, strategies or novel drugs are urgently required to protect against liver dysfunction in sepsis. In the present study, lipopolysaccharide (LPS) was used to establish a model of liver injury in vitro. The data demonstrated that pretreatment of L02 human normal hepatocytes with paeonol (PAE) alleviated LPS-induced cell injury and decreased the levels of alanine aminotransferase and aspartate transaminase, indicating a protective effect of PAE. Further experiments demonstrated that PAE increased LPS-decreased L02 cell viability, the levels of superoxide dismutase and Bcl-2 expression. PAE decreased LPS-increased cell apoptosis, intracellular reactive oxygen species and the expression levels of Bax and cleaved-caspase-3. PAE decreased LPS-promoted mitochondrial depolarization and nuclear translocation of NF-κB. In conclusion, PAE alleviated LPS-induced liver injury via alteration of mitochondrial function and NF-κB translocation. Therefore, PAE has potential for the treatment of sepsis. D.A. Spandidos 2021-11 2021-09-07 /pmc/articles/PMC8436227/ /pubmed/34498704 http://dx.doi.org/10.3892/mmr.2021.12419 Text en Copyright: © Xu et al. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by-nc/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Xu, Shouzhu
Xu, Jie
Hao, Ting
Yan, Yu
Zhang, Shihao
Li, Aihong
Shi, Chuandao
Liu, Qiling
Zhao, Jing
Paeonol alleviates lipopolysaccharide-induced hepatocytes injury through alteration of mitochondrial function and NF-κB translocation
title Paeonol alleviates lipopolysaccharide-induced hepatocytes injury through alteration of mitochondrial function and NF-κB translocation
title_full Paeonol alleviates lipopolysaccharide-induced hepatocytes injury through alteration of mitochondrial function and NF-κB translocation
title_fullStr Paeonol alleviates lipopolysaccharide-induced hepatocytes injury through alteration of mitochondrial function and NF-κB translocation
title_full_unstemmed Paeonol alleviates lipopolysaccharide-induced hepatocytes injury through alteration of mitochondrial function and NF-κB translocation
title_short Paeonol alleviates lipopolysaccharide-induced hepatocytes injury through alteration of mitochondrial function and NF-κB translocation
title_sort paeonol alleviates lipopolysaccharide-induced hepatocytes injury through alteration of mitochondrial function and nf-κb translocation
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8436227/
https://www.ncbi.nlm.nih.gov/pubmed/34498704
http://dx.doi.org/10.3892/mmr.2021.12419
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