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Shen-Kang protects against tacrolimus-induced renal injury
BACKGROUND/AIMS: Evidence suggests that Shen-Kang (SK), a traditional Chinese herbal medicine, protects against various types of renal injury. In this study, we evaluated whether SK treatment confers renoprotection in a rat model of chronic tacrolimus (TAC) nephropathy. METHODS: Rats were treated da...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Association of Internal Medicine
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6718754/ https://www.ncbi.nlm.nih.gov/pubmed/29432674 http://dx.doi.org/10.3904/kjim.2017.276 |
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author | Zhang, Long Ye Jin, Jian Luo, Kang Piao, Shang Guo Zheng, Hai Lan Jin, Ji Zhe Lim, Sun Woo Choi, Bum Soon Yang, Chul Woo Li, Can |
author_facet | Zhang, Long Ye Jin, Jian Luo, Kang Piao, Shang Guo Zheng, Hai Lan Jin, Ji Zhe Lim, Sun Woo Choi, Bum Soon Yang, Chul Woo Li, Can |
author_sort | Zhang, Long Ye |
collection | PubMed |
description | BACKGROUND/AIMS: Evidence suggests that Shen-Kang (SK), a traditional Chinese herbal medicine, protects against various types of renal injury. In this study, we evaluated whether SK treatment confers renoprotection in a rat model of chronic tacrolimus (TAC) nephropathy. METHODS: Rats were treated daily with TAC (1.5mg/kg, subcutaneously) and SK (450 mg/kg, intravenously) for 4 weeks. The effects of SK on TAC-induced renal injury were assessed by measuring renal function, urine albumin excretion, histopathology, inflammatory cell infiltration, expression of profibrotic (transforming growth factor β1 [TGF-β1] and TGF-β inducible gene-h3 [βig-h3]) and proinflammatory cytokines, oxidative stress, and apoptotic cell death. RESULTS: Administration of SK preserved glomerular integrity (fractional mesangial area and Wilms tumor 1-positive glomeruli), attenuated tubulointerstitial fibrosis, and reduced the number of ectodermal dysplasia 1-positive cells, and this was paralleled by improved urine albumin excretion and renal dysfunction. At the molecular level, SK treatment suppressed expression of TGF-β1/Smad2/3, βig-h3, and proinflammatory cytokines. Oxidative stress and apoptotic cell death were significantly decreased with SK treatment, and apoptosis-related genes were regulated toward cell survival (active caspase-3 and the B-cell lymphoma-2/Bcl2-associated X [Bcl-2/Bax] ratio). CONCLUSIONS: SK protects against TAC-induced renal injury. |
format | Online Article Text |
id | pubmed-6718754 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | The Korean Association of Internal Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-67187542019-09-06 Shen-Kang protects against tacrolimus-induced renal injury Zhang, Long Ye Jin, Jian Luo, Kang Piao, Shang Guo Zheng, Hai Lan Jin, Ji Zhe Lim, Sun Woo Choi, Bum Soon Yang, Chul Woo Li, Can Korean J Intern Med Original Article BACKGROUND/AIMS: Evidence suggests that Shen-Kang (SK), a traditional Chinese herbal medicine, protects against various types of renal injury. In this study, we evaluated whether SK treatment confers renoprotection in a rat model of chronic tacrolimus (TAC) nephropathy. METHODS: Rats were treated daily with TAC (1.5mg/kg, subcutaneously) and SK (450 mg/kg, intravenously) for 4 weeks. The effects of SK on TAC-induced renal injury were assessed by measuring renal function, urine albumin excretion, histopathology, inflammatory cell infiltration, expression of profibrotic (transforming growth factor β1 [TGF-β1] and TGF-β inducible gene-h3 [βig-h3]) and proinflammatory cytokines, oxidative stress, and apoptotic cell death. RESULTS: Administration of SK preserved glomerular integrity (fractional mesangial area and Wilms tumor 1-positive glomeruli), attenuated tubulointerstitial fibrosis, and reduced the number of ectodermal dysplasia 1-positive cells, and this was paralleled by improved urine albumin excretion and renal dysfunction. At the molecular level, SK treatment suppressed expression of TGF-β1/Smad2/3, βig-h3, and proinflammatory cytokines. Oxidative stress and apoptotic cell death were significantly decreased with SK treatment, and apoptosis-related genes were regulated toward cell survival (active caspase-3 and the B-cell lymphoma-2/Bcl2-associated X [Bcl-2/Bax] ratio). CONCLUSIONS: SK protects against TAC-induced renal injury. The Korean Association of Internal Medicine 2019-09 2018-02-12 /pmc/articles/PMC6718754/ /pubmed/29432674 http://dx.doi.org/10.3904/kjim.2017.276 Text en Copyright © 2019 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Zhang, Long Ye Jin, Jian Luo, Kang Piao, Shang Guo Zheng, Hai Lan Jin, Ji Zhe Lim, Sun Woo Choi, Bum Soon Yang, Chul Woo Li, Can Shen-Kang protects against tacrolimus-induced renal injury |
title | Shen-Kang protects against tacrolimus-induced renal injury |
title_full | Shen-Kang protects against tacrolimus-induced renal injury |
title_fullStr | Shen-Kang protects against tacrolimus-induced renal injury |
title_full_unstemmed | Shen-Kang protects against tacrolimus-induced renal injury |
title_short | Shen-Kang protects against tacrolimus-induced renal injury |
title_sort | shen-kang protects against tacrolimus-induced renal injury |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6718754/ https://www.ncbi.nlm.nih.gov/pubmed/29432674 http://dx.doi.org/10.3904/kjim.2017.276 |
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