Aristolochic acid induces chronic kidney disease in ace knockout mice

Background: Aristolochic acid I (AAI) is an extract from Chinese herbs that causes progressive interstitial nephritis. The aim of this research is to know whether chymases play the crucial role in AAI-induced nephropathy. Methods: The mice were treated with AAI via intraperitoneal injection and the...

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Autor principal:	Jia-Ping Wu
Formato:	article
Lenguaje:	EN
Publicado:	Wolters Kluwer Medknow Publications 2021
Materias:	aristolochic acid i chronic kidney disease chymases peptidyl-dipeptidase a renal insufficiency Medicine R
Acceso en línea:	https://doaj.org/article/c07f6ed69e00425f897df5aaea1442fc
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spelling	oai:doaj.org-article:c07f6ed69e00425f897df5aaea1442fc2021-11-12T10:11:33ZAristolochic acid induces chronic kidney disease in ace knockout mice2008-78022008-821310.4103/ijpvm.IJPVM_344_19https://doaj.org/article/c07f6ed69e00425f897df5aaea1442fc2021-01-01T00:00:00Zhttp://www.ijpvmjournal.net/article.asp?issn=2008-7802;year=2021;volume=12;issue=1;spage=151;epage=151;aulast=Wuhttps://doaj.org/toc/2008-7802https://doaj.org/toc/2008-8213Background: Aristolochic acid I (AAI) is an extract from Chinese herbs that causes progressive interstitial nephritis. The aim of this research is to know whether chymases play the crucial role in AAI-induced nephropathy. Methods: The mice were treated with AAI via intraperitoneal injection and the accumulated AAI dosages are 30 mg/kg of body weight for two, four, six, and eight weeks. The animals were sacrificed after another two or four weeks for nephropathy development. Collection of blood, urine, and kidney samples for the further biochemical analysis, hematoxylin–eosin (H and E) and Masson's trichrome stained to detected pathologic, and MMP2 and MMP9 activity assays. Results: After the treatment of AAI, of the mice, their body weights were decreased (P < 0.01), and concentration of creatinine and blood urea nitrogen (BUN) in serum (P < 0.01) and urine collection were increased (P < 0.01). In the renal tissue sections, high amount of inflammatory cells were found by H and E stain, and increased fibrosis in renal interstitial tissue were observed by Masson's trichrome stain. In mice kidney tissue, significantly increased chymase activity after treatment of AAI was found (P < 0.01), but ACE activity did not show significant changes. In ACE KO mice, increased MMP2 and decreased MMP9 activity were found in the AAI-treated mice compared with AAI-untreated control (P < 0.01). Conclusions: Moreover, it was also observed that the deficiency of ACE would accelerate the disease development of AAI-induced nephropathy. These results may help to know more information about the role of AAI-induced chronic kidney disease and can be applied in developing new drug targets for nephropathy.Jia-Ping WuWolters Kluwer Medknow Publicationsarticle aristolochic acid ichronic kidney diseasechymasespeptidyl-dipeptidase arenal insufficiency MedicineRENInternational Journal of Preventive Medicine, Vol 12, Iss 1, Pp 151-151 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	aristolochic acid i chronic kidney disease chymases peptidyl-dipeptidase a renal insufficiency Medicine R
spellingShingle	aristolochic acid i chronic kidney disease chymases peptidyl-dipeptidase a renal insufficiency Medicine R Jia-Ping Wu Aristolochic acid induces chronic kidney disease in ace knockout mice
description	Background: Aristolochic acid I (AAI) is an extract from Chinese herbs that causes progressive interstitial nephritis. The aim of this research is to know whether chymases play the crucial role in AAI-induced nephropathy. Methods: The mice were treated with AAI via intraperitoneal injection and the accumulated AAI dosages are 30 mg/kg of body weight for two, four, six, and eight weeks. The animals were sacrificed after another two or four weeks for nephropathy development. Collection of blood, urine, and kidney samples for the further biochemical analysis, hematoxylin–eosin (H and E) and Masson's trichrome stained to detected pathologic, and MMP2 and MMP9 activity assays. Results: After the treatment of AAI, of the mice, their body weights were decreased (P < 0.01), and concentration of creatinine and blood urea nitrogen (BUN) in serum (P < 0.01) and urine collection were increased (P < 0.01). In the renal tissue sections, high amount of inflammatory cells were found by H and E stain, and increased fibrosis in renal interstitial tissue were observed by Masson's trichrome stain. In mice kidney tissue, significantly increased chymase activity after treatment of AAI was found (P < 0.01), but ACE activity did not show significant changes. In ACE KO mice, increased MMP2 and decreased MMP9 activity were found in the AAI-treated mice compared with AAI-untreated control (P < 0.01). Conclusions: Moreover, it was also observed that the deficiency of ACE would accelerate the disease development of AAI-induced nephropathy. These results may help to know more information about the role of AAI-induced chronic kidney disease and can be applied in developing new drug targets for nephropathy.
format	article
author	Jia-Ping Wu
author_facet	Jia-Ping Wu
author_sort	Jia-Ping Wu
title	Aristolochic acid induces chronic kidney disease in ace knockout mice
title_short	Aristolochic acid induces chronic kidney disease in ace knockout mice
title_full	Aristolochic acid induces chronic kidney disease in ace knockout mice
title_fullStr	Aristolochic acid induces chronic kidney disease in ace knockout mice
title_full_unstemmed	Aristolochic acid induces chronic kidney disease in ace knockout mice
title_sort	aristolochic acid induces chronic kidney disease in ace knockout mice
publisher	Wolters Kluwer Medknow Publications
publishDate	2021
url	https://doaj.org/article/c07f6ed69e00425f897df5aaea1442fc
work_keys_str_mv	AT jiapingwu aristolochicacidinduceschronickidneydiseaseinaceknockoutmice
_version_	1718431015239680000

Aristolochic acid induces chronic kidney disease in ace knockout mice

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