Exploring the effects of hypoxia and reoxygenation time on hepatocyte apoptosis and inflammation.

Hepatic Ischemia-Reperfusion Injury (HIRI) is an unavoidable pathological process during liver surgeries such as liver transplantation and hepatic resection, which involves a complex set of molecular and cellular mechanisms. The mechanisms of HIRI may involve a variety of biological processes in whi...

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Main Authors: Xinlu Xu, Tanfang Zhou, Alimu Tulahong, Rexiati Ruze, Yingmei Shao
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2024-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0310535
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author Xinlu Xu
Tanfang Zhou
Alimu Tulahong
Rexiati Ruze
Yingmei Shao
author_facet Xinlu Xu
Tanfang Zhou
Alimu Tulahong
Rexiati Ruze
Yingmei Shao
author_sort Xinlu Xu
collection DOAJ
description Hepatic Ischemia-Reperfusion Injury (HIRI) is an unavoidable pathological process during liver surgeries such as liver transplantation and hepatic resection, which involves a complex set of molecular and cellular mechanisms. The mechanisms of HIRI may involve a variety of biological processes in which inflammation and apoptosis play a central role. Therefore, it is crucial to deeply investigate the effects of different hypoxia and reoxygenation times on the construction of an in vitro model of hepatic ischemia-reperfusion injury. The human normal liver cell line HL-7702 IRI model was constructed by hypoxia chamber, and the inflammation and apoptosis focal levels of cells were detected by enzyme-linked immunosorbent assay, western blot and quantitative reverse transcription polymerase chain reaction. When 12-hour reoxygenation time was fixed, the inflammation and apoptosis indexes of HIRI model increased with the prolongation of hypoxia time (6, 12 and 24 hours). These indices reached highest level in the model group of 24-hour fixed hypoxia and 12-hour reoxygenation. Inflammation and apoptosis indices were significantly higher in the model group of 24-hours fixed hypoxia and 12-hours reoxygenation than in the group of 6 and 24 hours of reoxygenation. Taken together, the findings from this research demonstrated that during hypoxia phase, cells exhibited a clear time-dependent response of inflammation and cell death; on the contrary, during the reoxygenation phase, the cellular damage was not monotonically incremental, but showed an inverted U-shaped dynamic pattern. The present study reveals in depth the dynamic changes of cellular responses under hypoxia and reoxygenation conditions, providing us with an important theoretical basis to guide the selection and optimization of in vitro experimental models.
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spelling doaj-art-e567c161168049de84c98a9098f1c02a2024-11-25T05:31:25ZengPublic Library of Science (PLoS)PLoS ONE1932-62032024-01-011911e031053510.1371/journal.pone.0310535Exploring the effects of hypoxia and reoxygenation time on hepatocyte apoptosis and inflammation.Xinlu XuTanfang ZhouAlimu TulahongRexiati RuzeYingmei ShaoHepatic Ischemia-Reperfusion Injury (HIRI) is an unavoidable pathological process during liver surgeries such as liver transplantation and hepatic resection, which involves a complex set of molecular and cellular mechanisms. The mechanisms of HIRI may involve a variety of biological processes in which inflammation and apoptosis play a central role. Therefore, it is crucial to deeply investigate the effects of different hypoxia and reoxygenation times on the construction of an in vitro model of hepatic ischemia-reperfusion injury. The human normal liver cell line HL-7702 IRI model was constructed by hypoxia chamber, and the inflammation and apoptosis focal levels of cells were detected by enzyme-linked immunosorbent assay, western blot and quantitative reverse transcription polymerase chain reaction. When 12-hour reoxygenation time was fixed, the inflammation and apoptosis indexes of HIRI model increased with the prolongation of hypoxia time (6, 12 and 24 hours). These indices reached highest level in the model group of 24-hour fixed hypoxia and 12-hour reoxygenation. Inflammation and apoptosis indices were significantly higher in the model group of 24-hours fixed hypoxia and 12-hours reoxygenation than in the group of 6 and 24 hours of reoxygenation. Taken together, the findings from this research demonstrated that during hypoxia phase, cells exhibited a clear time-dependent response of inflammation and cell death; on the contrary, during the reoxygenation phase, the cellular damage was not monotonically incremental, but showed an inverted U-shaped dynamic pattern. The present study reveals in depth the dynamic changes of cellular responses under hypoxia and reoxygenation conditions, providing us with an important theoretical basis to guide the selection and optimization of in vitro experimental models.https://doi.org/10.1371/journal.pone.0310535
spellingShingle Xinlu Xu
Tanfang Zhou
Alimu Tulahong
Rexiati Ruze
Yingmei Shao
Exploring the effects of hypoxia and reoxygenation time on hepatocyte apoptosis and inflammation.
PLoS ONE
title Exploring the effects of hypoxia and reoxygenation time on hepatocyte apoptosis and inflammation.
title_full Exploring the effects of hypoxia and reoxygenation time on hepatocyte apoptosis and inflammation.
title_fullStr Exploring the effects of hypoxia and reoxygenation time on hepatocyte apoptosis and inflammation.
title_full_unstemmed Exploring the effects of hypoxia and reoxygenation time on hepatocyte apoptosis and inflammation.
title_short Exploring the effects of hypoxia and reoxygenation time on hepatocyte apoptosis and inflammation.
title_sort exploring the effects of hypoxia and reoxygenation time on hepatocyte apoptosis and inflammation
url https://doi.org/10.1371/journal.pone.0310535
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AT rexiatiruze exploringtheeffectsofhypoxiaandreoxygenationtimeonhepatocyteapoptosisandinflammation
AT yingmeishao exploringtheeffectsofhypoxiaandreoxygenationtimeonhepatocyteapoptosisandinflammation