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Protective Effect of Astragaloside IV on Hepatic Injury Induced by Iron Overload

Suitable content of iron is essential for human body, but iron overload is associated with many kinds of diseases including chronic liver damage. Recently, researchers find that iron overload promotes hepatocyte autophagy and apoptosis. However, the mechanism of iron overload in liver damage remains...

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Autores principales: Xie, Dongyu, Zhou, Ping, Liu, Lin, Jiang, Wenjing, Xie, Haina, Zhang, Liang, Xie, Donghao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683835/
https://www.ncbi.nlm.nih.gov/pubmed/31428632
http://dx.doi.org/10.1155/2019/3103946
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author Xie, Dongyu
Zhou, Ping
Liu, Lin
Jiang, Wenjing
Xie, Haina
Zhang, Liang
Xie, Donghao
author_facet Xie, Dongyu
Zhou, Ping
Liu, Lin
Jiang, Wenjing
Xie, Haina
Zhang, Liang
Xie, Donghao
author_sort Xie, Dongyu
collection PubMed
description Suitable content of iron is essential for human body, but iron overload is associated with many kinds of diseases including chronic liver damage. Recently, researchers find that iron overload promotes hepatocyte autophagy and apoptosis. However, the mechanism of iron overload in liver damage remains unclear. In this study, Lo2 cells were selected as the research object, iron dextran was a model drug, and astragaloside IV was a therapeutic drug to explore the role of iron overload. MTT assay and Annexin/PI double staining were used to measure cell viability and apoptosis. Ultrastructure was observed by transmission electron microscopy. The expression levels of apoptosis and autophagy-related proteins were determined by real-time PCR and Western Blot. The results showed that iron dextran could significantly inhibit Lo2 cell viability and increase the apoptosis rate, while astragaloside IV could reverse the inhibition of Lo2 cell viability and decrease the apoptosis rate. Transmission electron microscopy showed a significant increase in the number of autophagosomes after administration of iron dextran, and the application of astragaloside IV reduced the production of autophagosomes. LC3II/I was significantly upregulated in the model group but decreased in the astragaloside IV treatment group, and P62 showed the opposite trend. Iron dextran significantly upregulated the expression of Bax and downregulated Bcl2, while astragaloside IV reversed this trend. Finally, the inhibition of hepcidin caused by iron dextran was counteracted by astragaloside IV. In conclusion, the experimental results show that the iron overload model mainly induces excessive autophagy and apoptosis of hepatocytes, thus causing damage to hepatocytes, but astragaloside IV plays a certain therapeutic role in reversing this damage.
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spelling pubmed-66838352019-08-19 Protective Effect of Astragaloside IV on Hepatic Injury Induced by Iron Overload Xie, Dongyu Zhou, Ping Liu, Lin Jiang, Wenjing Xie, Haina Zhang, Liang Xie, Donghao Biomed Res Int Research Article Suitable content of iron is essential for human body, but iron overload is associated with many kinds of diseases including chronic liver damage. Recently, researchers find that iron overload promotes hepatocyte autophagy and apoptosis. However, the mechanism of iron overload in liver damage remains unclear. In this study, Lo2 cells were selected as the research object, iron dextran was a model drug, and astragaloside IV was a therapeutic drug to explore the role of iron overload. MTT assay and Annexin/PI double staining were used to measure cell viability and apoptosis. Ultrastructure was observed by transmission electron microscopy. The expression levels of apoptosis and autophagy-related proteins were determined by real-time PCR and Western Blot. The results showed that iron dextran could significantly inhibit Lo2 cell viability and increase the apoptosis rate, while astragaloside IV could reverse the inhibition of Lo2 cell viability and decrease the apoptosis rate. Transmission electron microscopy showed a significant increase in the number of autophagosomes after administration of iron dextran, and the application of astragaloside IV reduced the production of autophagosomes. LC3II/I was significantly upregulated in the model group but decreased in the astragaloside IV treatment group, and P62 showed the opposite trend. Iron dextran significantly upregulated the expression of Bax and downregulated Bcl2, while astragaloside IV reversed this trend. Finally, the inhibition of hepcidin caused by iron dextran was counteracted by astragaloside IV. In conclusion, the experimental results show that the iron overload model mainly induces excessive autophagy and apoptosis of hepatocytes, thus causing damage to hepatocytes, but astragaloside IV plays a certain therapeutic role in reversing this damage. Hindawi 2019-07-25 /pmc/articles/PMC6683835/ /pubmed/31428632 http://dx.doi.org/10.1155/2019/3103946 Text en Copyright © 2019 Dongyu Xie 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
Xie, Dongyu
Zhou, Ping
Liu, Lin
Jiang, Wenjing
Xie, Haina
Zhang, Liang
Xie, Donghao
Protective Effect of Astragaloside IV on Hepatic Injury Induced by Iron Overload
title Protective Effect of Astragaloside IV on Hepatic Injury Induced by Iron Overload
title_full Protective Effect of Astragaloside IV on Hepatic Injury Induced by Iron Overload
title_fullStr Protective Effect of Astragaloside IV on Hepatic Injury Induced by Iron Overload
title_full_unstemmed Protective Effect of Astragaloside IV on Hepatic Injury Induced by Iron Overload
title_short Protective Effect of Astragaloside IV on Hepatic Injury Induced by Iron Overload
title_sort protective effect of astragaloside iv on hepatic injury induced by iron overload
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683835/
https://www.ncbi.nlm.nih.gov/pubmed/31428632
http://dx.doi.org/10.1155/2019/3103946
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