Cargando…

Cul4a attenuates LPS-induced acute kidney injury via blocking NF-kB signaling pathway in sepsis

BACKGROUND: Acute kidney injury (AKI) is a common disease that can develop into end-stage kidney disease. Sepsis is one of the main causes of AKI. Currently, there is no satisfactory way to treat septic AKI. Therefore, we have shown the protective function of Cul4a in septic AKI and its molecular me...

Descripción completa

Detalles Bibliográficos
Autores principales: Zhao, Jing, Duan, Qiuxia, Dong, Cuihong, Cui, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Society of Medical Biochemists of Serbia, Belgrade 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9069243/
https://www.ncbi.nlm.nih.gov/pubmed/35611245
http://dx.doi.org/10.5937/jomb0-33096
_version_ 1784700389150425088
author Zhao, Jing
Duan, Qiuxia
Dong, Cuihong
Cui, Jing
author_facet Zhao, Jing
Duan, Qiuxia
Dong, Cuihong
Cui, Jing
author_sort Zhao, Jing
collection PubMed
description BACKGROUND: Acute kidney injury (AKI) is a common disease that can develop into end-stage kidney disease. Sepsis is one of the main causes of AKI. Currently, there is no satisfactory way to treat septic AKI. Therefore, we have shown the protective function of Cul4a in septic AKI and its molecular mechanism. METHODS: The cellular and animal models of septic AKI were established by using lipopolysaccharide (LPS). Western blot (WB) was employed to analyze Cul4a expression. RT-qPCR was employed to test the expression of Cul4a, SOD1, SOD2, GPX1, CAT, IL-6, TNF-a, Bcl-2, IL1b, Bax and KIM-1 mRNA. ELISA was performed to detect the contents of inflammatory factors and LDH. CCK-8 was utilized to detect cell viability. Flow cytometry was utilized to analyze the apoptosis. DHE-ROS kit was used to detect the content of ROS. RESULTS: Cul4a was down-regulated in cellular and animal models of septic AKI. Oxidative stress is obviously induced by LPS, as well as apoptosis and inflammation. However, these can be significantly inhibited by up-regulating Cul4a. Moreover, LPS induced the activation of the NF-kB pathway, which could also be inhibited by overexpression of Cul4a. CONCLUSIONS: Cul4awas found to be a protective factor in septic AKI, which could inhibit LPS-induced oxidative stress, apoptosis and inflammation of HK-2 cells by inhibiting the NF-kB pathway.
format Online
Article
Text
id pubmed-9069243
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Society of Medical Biochemists of Serbia, Belgrade
record_format MEDLINE/PubMed
spelling pubmed-90692432022-05-23 Cul4a attenuates LPS-induced acute kidney injury via blocking NF-kB signaling pathway in sepsis Zhao, Jing Duan, Qiuxia Dong, Cuihong Cui, Jing J Med Biochem Original Paper BACKGROUND: Acute kidney injury (AKI) is a common disease that can develop into end-stage kidney disease. Sepsis is one of the main causes of AKI. Currently, there is no satisfactory way to treat septic AKI. Therefore, we have shown the protective function of Cul4a in septic AKI and its molecular mechanism. METHODS: The cellular and animal models of septic AKI were established by using lipopolysaccharide (LPS). Western blot (WB) was employed to analyze Cul4a expression. RT-qPCR was employed to test the expression of Cul4a, SOD1, SOD2, GPX1, CAT, IL-6, TNF-a, Bcl-2, IL1b, Bax and KIM-1 mRNA. ELISA was performed to detect the contents of inflammatory factors and LDH. CCK-8 was utilized to detect cell viability. Flow cytometry was utilized to analyze the apoptosis. DHE-ROS kit was used to detect the content of ROS. RESULTS: Cul4a was down-regulated in cellular and animal models of septic AKI. Oxidative stress is obviously induced by LPS, as well as apoptosis and inflammation. However, these can be significantly inhibited by up-regulating Cul4a. Moreover, LPS induced the activation of the NF-kB pathway, which could also be inhibited by overexpression of Cul4a. CONCLUSIONS: Cul4awas found to be a protective factor in septic AKI, which could inhibit LPS-induced oxidative stress, apoptosis and inflammation of HK-2 cells by inhibiting the NF-kB pathway. Society of Medical Biochemists of Serbia, Belgrade 2022-02-02 2022-02-02 /pmc/articles/PMC9069243/ /pubmed/35611245 http://dx.doi.org/10.5937/jomb0-33096 Text en 2022 Jing Zhao, Qiuxia Duan, Cuihong Dong, Jing Cui, published by CEON/CEES https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 License.
spellingShingle Original Paper
Zhao, Jing
Duan, Qiuxia
Dong, Cuihong
Cui, Jing
Cul4a attenuates LPS-induced acute kidney injury via blocking NF-kB signaling pathway in sepsis
title Cul4a attenuates LPS-induced acute kidney injury via blocking NF-kB signaling pathway in sepsis
title_full Cul4a attenuates LPS-induced acute kidney injury via blocking NF-kB signaling pathway in sepsis
title_fullStr Cul4a attenuates LPS-induced acute kidney injury via blocking NF-kB signaling pathway in sepsis
title_full_unstemmed Cul4a attenuates LPS-induced acute kidney injury via blocking NF-kB signaling pathway in sepsis
title_short Cul4a attenuates LPS-induced acute kidney injury via blocking NF-kB signaling pathway in sepsis
title_sort cul4a attenuates lps-induced acute kidney injury via blocking nf-kb signaling pathway in sepsis
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9069243/
https://www.ncbi.nlm.nih.gov/pubmed/35611245
http://dx.doi.org/10.5937/jomb0-33096
work_keys_str_mv AT zhaojing cul4aattenuateslpsinducedacutekidneyinjuryviablockingnfkbsignalingpathwayinsepsis
AT duanqiuxia cul4aattenuateslpsinducedacutekidneyinjuryviablockingnfkbsignalingpathwayinsepsis
AT dongcuihong cul4aattenuateslpsinducedacutekidneyinjuryviablockingnfkbsignalingpathwayinsepsis
AT cuijing cul4aattenuateslpsinducedacutekidneyinjuryviablockingnfkbsignalingpathwayinsepsis