Artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice

Abstract The kidney is a high-energy demand organ rich in mitochondria especially renal tubular cells. Emerging evidence suggests that mitochondrial dysfunction, redox imbalance and kidney injury are interconnected. Artemether has biological effects by targeting mitochondria and exhibits potential t...

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Autores principales: Pengxun Han, Yuchun Cai, Yao Wang, Wenci Weng, Yinghui Chen, Menghua Wang, Hongyue Zhan, Xuewen Yu, Taifen Wang, Mumin Shao, Huili Sun
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/dbc88c2de4a048b7bc51329955172b69
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spelling oai:doaj.org-article:dbc88c2de4a048b7bc51329955172b692021-12-02T14:12:46ZArtemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice10.1038/s41598-020-80298-x2045-2322https://doaj.org/article/dbc88c2de4a048b7bc51329955172b692021-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-80298-xhttps://doaj.org/toc/2045-2322Abstract The kidney is a high-energy demand organ rich in mitochondria especially renal tubular cells. Emerging evidence suggests that mitochondrial dysfunction, redox imbalance and kidney injury are interconnected. Artemether has biological effects by targeting mitochondria and exhibits potential therapeutic value for kidney disease. However, the underlying molecular mechanisms have not been fully elucidated. This study was performed to determine the effects of artemether on Adriamycin-induced nephropathy and the potential mechanisms were also investigated. In vivo, an Adriamycin nephropathy mouse model was established, and mice were treated with or without artemether for 2 weeks. In vitro, NRK-52E cells were stimulated with TGF-β1 and treated with or without artemether for 24 h. Then renal damage and cell changes were evaluated. The results demonstrated that artemether reduced urinary protein excretion, recovered podocyte alterations, attenuated pathological changes and alleviated renal tubular injury. Artemether also downregulated TGF-β1 mRNA expression levels, inhibited tubular proliferation, restored tubular cell phenotypes and suppressed proliferation-related signalling pathways. In addition, artemether restored renal redox imbalance, increased mtDNA copy number and improved mitochondrial function. In summary, we provided initial evidence that artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice. Artemether may be a promising agent for the treatment kidney disease.Pengxun HanYuchun CaiYao WangWenci WengYinghui ChenMenghua WangHongyue ZhanXuewen YuTaifen WangMumin ShaoHuili SunNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Pengxun Han
Yuchun Cai
Yao Wang
Wenci Weng
Yinghui Chen
Menghua Wang
Hongyue Zhan
Xuewen Yu
Taifen Wang
Mumin Shao
Huili Sun
Artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice
description Abstract The kidney is a high-energy demand organ rich in mitochondria especially renal tubular cells. Emerging evidence suggests that mitochondrial dysfunction, redox imbalance and kidney injury are interconnected. Artemether has biological effects by targeting mitochondria and exhibits potential therapeutic value for kidney disease. However, the underlying molecular mechanisms have not been fully elucidated. This study was performed to determine the effects of artemether on Adriamycin-induced nephropathy and the potential mechanisms were also investigated. In vivo, an Adriamycin nephropathy mouse model was established, and mice were treated with or without artemether for 2 weeks. In vitro, NRK-52E cells were stimulated with TGF-β1 and treated with or without artemether for 24 h. Then renal damage and cell changes were evaluated. The results demonstrated that artemether reduced urinary protein excretion, recovered podocyte alterations, attenuated pathological changes and alleviated renal tubular injury. Artemether also downregulated TGF-β1 mRNA expression levels, inhibited tubular proliferation, restored tubular cell phenotypes and suppressed proliferation-related signalling pathways. In addition, artemether restored renal redox imbalance, increased mtDNA copy number and improved mitochondrial function. In summary, we provided initial evidence that artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice. Artemether may be a promising agent for the treatment kidney disease.
format article
author Pengxun Han
Yuchun Cai
Yao Wang
Wenci Weng
Yinghui Chen
Menghua Wang
Hongyue Zhan
Xuewen Yu
Taifen Wang
Mumin Shao
Huili Sun
author_facet Pengxun Han
Yuchun Cai
Yao Wang
Wenci Weng
Yinghui Chen
Menghua Wang
Hongyue Zhan
Xuewen Yu
Taifen Wang
Mumin Shao
Huili Sun
author_sort Pengxun Han
title Artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice
title_short Artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice
title_full Artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice
title_fullStr Artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice
title_full_unstemmed Artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in Adriamycin nephropathy in mice
title_sort artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in adriamycin nephropathy in mice
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/dbc88c2de4a048b7bc51329955172b69
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