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CST3 alleviates bilirubin-induced neurocytes’ damage by promoting autophagy

High concentrations of unconjugated bilirubin (UCB) have toxic effects. The aim of our study was to find a way to elevate UCB tolerance or inhibit its toxicity in neurocytes. It has been reported that cystatin C (CST3) concentrations have a significant positive correlation with total bilirubin (TB)...

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Autores principales: Li, Zhenkun, Du, Yating
Formato: Online Artículo Texto
Lenguaje:English
Publicado: De Gruyter 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10579785/
https://www.ncbi.nlm.nih.gov/pubmed/37854583
http://dx.doi.org/10.1515/tnsci-2022-0314
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author Li, Zhenkun
Du, Yating
author_facet Li, Zhenkun
Du, Yating
author_sort Li, Zhenkun
collection PubMed
description High concentrations of unconjugated bilirubin (UCB) have toxic effects. The aim of our study was to find a way to elevate UCB tolerance or inhibit its toxicity in neurocytes. It has been reported that cystatin C (CST3) concentrations have a significant positive correlation with total bilirubin (TB) levels and a negative correlation with albumin levels. In addition, CST3 can directly bind UCB, decrease human umbilical vein endothelial cells’ permeability, improve blood–brain barrier integrity after ischemic brain injury in mice, and induce autophagy. We hypothesized that CST3 could increase the solubility of UCB, decrease permeability of neurocytes, induce autophagy of neurocytes, and alleviate bilirubin-induced damage. To verify our hypothesis, we measured TB and conjugated bilirubin levels, and the permeability and autophagy of neurocytes treated with UCB and CST3. Our findings suggest that CST3 can protect against UCB-induced damage in neurocytes and that autophagy played an important role in this process.
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spelling pubmed-105797852023-10-18 CST3 alleviates bilirubin-induced neurocytes’ damage by promoting autophagy Li, Zhenkun Du, Yating Transl Neurosci Research Article High concentrations of unconjugated bilirubin (UCB) have toxic effects. The aim of our study was to find a way to elevate UCB tolerance or inhibit its toxicity in neurocytes. It has been reported that cystatin C (CST3) concentrations have a significant positive correlation with total bilirubin (TB) levels and a negative correlation with albumin levels. In addition, CST3 can directly bind UCB, decrease human umbilical vein endothelial cells’ permeability, improve blood–brain barrier integrity after ischemic brain injury in mice, and induce autophagy. We hypothesized that CST3 could increase the solubility of UCB, decrease permeability of neurocytes, induce autophagy of neurocytes, and alleviate bilirubin-induced damage. To verify our hypothesis, we measured TB and conjugated bilirubin levels, and the permeability and autophagy of neurocytes treated with UCB and CST3. Our findings suggest that CST3 can protect against UCB-induced damage in neurocytes and that autophagy played an important role in this process. De Gruyter 2023-10-16 /pmc/articles/PMC10579785/ /pubmed/37854583 http://dx.doi.org/10.1515/tnsci-2022-0314 Text en © 2023 the author(s), published by De Gruyter https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License.
spellingShingle Research Article
Li, Zhenkun
Du, Yating
CST3 alleviates bilirubin-induced neurocytes’ damage by promoting autophagy
title CST3 alleviates bilirubin-induced neurocytes’ damage by promoting autophagy
title_full CST3 alleviates bilirubin-induced neurocytes’ damage by promoting autophagy
title_fullStr CST3 alleviates bilirubin-induced neurocytes’ damage by promoting autophagy
title_full_unstemmed CST3 alleviates bilirubin-induced neurocytes’ damage by promoting autophagy
title_short CST3 alleviates bilirubin-induced neurocytes’ damage by promoting autophagy
title_sort cst3 alleviates bilirubin-induced neurocytes’ damage by promoting autophagy
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10579785/
https://www.ncbi.nlm.nih.gov/pubmed/37854583
http://dx.doi.org/10.1515/tnsci-2022-0314
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