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Treatment with irbesatan may improve slit diaphragm alterations in rats with adriamycin-induced nephropathy
OBJECTIVE: The study aimed to evaluate the effects of oral administration of irbesartan in adriamycin-induced nephropathy considering laboratory changes, kidney histology, and expression of proteins related to slit diaphragm and cytoskeleton of the podocyte. METHODS: The animals were divided into co...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5843943/ https://www.ncbi.nlm.nih.gov/pubmed/27169889 http://dx.doi.org/10.1177/1470320316646884 |
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author | Wang, Na Wei, Ri-bao Li, Ping Li, Qing-ping Yang, Xi Yang, Yue Huang, Meng-jie Wang, Rui Yin, Zhong Lv, Yang Chen, Xiang-mei |
author_facet | Wang, Na Wei, Ri-bao Li, Ping Li, Qing-ping Yang, Xi Yang, Yue Huang, Meng-jie Wang, Rui Yin, Zhong Lv, Yang Chen, Xiang-mei |
author_sort | Wang, Na |
collection | PubMed |
description | OBJECTIVE: The study aimed to evaluate the effects of oral administration of irbesartan in adriamycin-induced nephropathy considering laboratory changes, kidney histology, and expression of proteins related to slit diaphragm and cytoskeleton of the podocyte. METHODS: The animals were divided into control, model, methylprednisolone (MP), and irbesartan groups. The 24-hour urinary protein and biochemical indicators were determined, and renal pathological changes were observed. The mRNA and protein expression of nephrin, podocin, CD2-associated protein (CD2AP), and desmin in the kidney tissue were analyzed. RESULTS: The urinary protein excretion levels in the MP and irbesartan groups were lower than those in the model group (p<0.01). Electron microscopy showed that fusion of the glomerular foot processes of the rats in the irbesartan group was significantly reduced. The mRNA and protein expression levels of nephrin and podocin in the renal tissue in the MP and irbesartan groups were up-regulated compared with the model group (p<0.05), whereas the mRNA and protein expression levels of CD2AP and desmin were significantly down-regulated (p<0.01). CONCLUSIONS: For rats with adriamycin-induced nephropathy, irbesartan could significantly reduce proteinuria. As a possible mechanism, irbesartan may improve the slit diaphragm protein of the glomerular podocyte and stabilize the cytoskeleton of the podocyte. |
format | Online Article Text |
id | pubmed-5843943 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-58439432018-03-20 Treatment with irbesatan may improve slit diaphragm alterations in rats with adriamycin-induced nephropathy Wang, Na Wei, Ri-bao Li, Ping Li, Qing-ping Yang, Xi Yang, Yue Huang, Meng-jie Wang, Rui Yin, Zhong Lv, Yang Chen, Xiang-mei J Renin Angiotensin Aldosterone Syst Original Article OBJECTIVE: The study aimed to evaluate the effects of oral administration of irbesartan in adriamycin-induced nephropathy considering laboratory changes, kidney histology, and expression of proteins related to slit diaphragm and cytoskeleton of the podocyte. METHODS: The animals were divided into control, model, methylprednisolone (MP), and irbesartan groups. The 24-hour urinary protein and biochemical indicators were determined, and renal pathological changes were observed. The mRNA and protein expression of nephrin, podocin, CD2-associated protein (CD2AP), and desmin in the kidney tissue were analyzed. RESULTS: The urinary protein excretion levels in the MP and irbesartan groups were lower than those in the model group (p<0.01). Electron microscopy showed that fusion of the glomerular foot processes of the rats in the irbesartan group was significantly reduced. The mRNA and protein expression levels of nephrin and podocin in the renal tissue in the MP and irbesartan groups were up-regulated compared with the model group (p<0.05), whereas the mRNA and protein expression levels of CD2AP and desmin were significantly down-regulated (p<0.01). CONCLUSIONS: For rats with adriamycin-induced nephropathy, irbesartan could significantly reduce proteinuria. As a possible mechanism, irbesartan may improve the slit diaphragm protein of the glomerular podocyte and stabilize the cytoskeleton of the podocyte. SAGE Publications 2016-05-09 /pmc/articles/PMC5843943/ /pubmed/27169889 http://dx.doi.org/10.1177/1470320316646884 Text en © The Author(s) 2016 http://creativecommons.org/licenses/by-nc/3.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page(https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Article Wang, Na Wei, Ri-bao Li, Ping Li, Qing-ping Yang, Xi Yang, Yue Huang, Meng-jie Wang, Rui Yin, Zhong Lv, Yang Chen, Xiang-mei Treatment with irbesatan may improve slit diaphragm alterations in rats with adriamycin-induced nephropathy |
title | Treatment with irbesatan may improve slit diaphragm alterations in rats with adriamycin-induced nephropathy |
title_full | Treatment with irbesatan may improve slit diaphragm alterations in rats with adriamycin-induced nephropathy |
title_fullStr | Treatment with irbesatan may improve slit diaphragm alterations in rats with adriamycin-induced nephropathy |
title_full_unstemmed | Treatment with irbesatan may improve slit diaphragm alterations in rats with adriamycin-induced nephropathy |
title_short | Treatment with irbesatan may improve slit diaphragm alterations in rats with adriamycin-induced nephropathy |
title_sort | treatment with irbesatan may improve slit diaphragm alterations in rats with adriamycin-induced nephropathy |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5843943/ https://www.ncbi.nlm.nih.gov/pubmed/27169889 http://dx.doi.org/10.1177/1470320316646884 |
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