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Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway

Objectives: To investigate the protective effect of different atorvastatin doses on contrast-induced acute kidney injury and the related mechanism. Methods: Healthy male Sprague–Dawley (SD) rats were randomly divided into the blank control group, experimental control group and different-dose atorvas...

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Autores principales: Yue, Rongzheng, Zuo, Chuan, Zeng, Jing, Su, Baihai, Tao, Ye, Huang, Songmin, Zeng, Rui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6447912/
https://www.ncbi.nlm.nih.gov/pubmed/28805489
http://dx.doi.org/10.1080/0886022X.2017.1361838
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author Yue, Rongzheng
Zuo, Chuan
Zeng, Jing
Su, Baihai
Tao, Ye
Huang, Songmin
Zeng, Rui
author_facet Yue, Rongzheng
Zuo, Chuan
Zeng, Jing
Su, Baihai
Tao, Ye
Huang, Songmin
Zeng, Rui
author_sort Yue, Rongzheng
collection PubMed
description Objectives: To investigate the protective effect of different atorvastatin doses on contrast-induced acute kidney injury and the related mechanism. Methods: Healthy male Sprague–Dawley (SD) rats were randomly divided into the blank control group, experimental control group and different-dose atorvastatin groups. A rat model of contrast-induced acute kidney injury was established. We detected changes in serum creatinine (Scr) and blood urea nitrogen (BUN) before and after model establishment, observed and scored renal tubular injury, analyzed rat renal cell apoptosis, and measure the expression of signal pathway proteins and downstream inflammatory factors. Results: After contrast agent injection, the Scr and BUN levels of the experimental control group were significantly increased, the different doses applied in the atorvastatin group significantly reduced the Scr and BUN levels (p < .05) and ameliorated the contrast-induced acute kidney injury (p < .05) and significantly reduced Toll-like receptor 4 (TLR4), Myeloid differentiation factor 88 (Myd88), and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) protein expression and relative mRNA expression levels (p < .05) and significantly decreased expression levels of downstream inflammatory factors (p < .05). Conclusion: Different atorvastatin doses have protective effects on contrast-induced acute renal tubular injury in rats, possibly by targeting TLR4, suppressing TLR4 expression, regulating the TLR4/Myd88 signaling pathway, and inhibiting the expression of downstream inflammatory factors.
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spelling pubmed-64479122019-04-12 Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway Yue, Rongzheng Zuo, Chuan Zeng, Jing Su, Baihai Tao, Ye Huang, Songmin Zeng, Rui Ren Fail Laboratory Study Objectives: To investigate the protective effect of different atorvastatin doses on contrast-induced acute kidney injury and the related mechanism. Methods: Healthy male Sprague–Dawley (SD) rats were randomly divided into the blank control group, experimental control group and different-dose atorvastatin groups. A rat model of contrast-induced acute kidney injury was established. We detected changes in serum creatinine (Scr) and blood urea nitrogen (BUN) before and after model establishment, observed and scored renal tubular injury, analyzed rat renal cell apoptosis, and measure the expression of signal pathway proteins and downstream inflammatory factors. Results: After contrast agent injection, the Scr and BUN levels of the experimental control group were significantly increased, the different doses applied in the atorvastatin group significantly reduced the Scr and BUN levels (p < .05) and ameliorated the contrast-induced acute kidney injury (p < .05) and significantly reduced Toll-like receptor 4 (TLR4), Myeloid differentiation factor 88 (Myd88), and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) protein expression and relative mRNA expression levels (p < .05) and significantly decreased expression levels of downstream inflammatory factors (p < .05). Conclusion: Different atorvastatin doses have protective effects on contrast-induced acute renal tubular injury in rats, possibly by targeting TLR4, suppressing TLR4 expression, regulating the TLR4/Myd88 signaling pathway, and inhibiting the expression of downstream inflammatory factors. Taylor & Francis 2017-08-14 /pmc/articles/PMC6447912/ /pubmed/28805489 http://dx.doi.org/10.1080/0886022X.2017.1361838 Text en © 2017 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Laboratory Study
Yue, Rongzheng
Zuo, Chuan
Zeng, Jing
Su, Baihai
Tao, Ye
Huang, Songmin
Zeng, Rui
Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway
title Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway
title_full Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway
title_fullStr Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway
title_full_unstemmed Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway
title_short Atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for TLR4/MyD88 signaling pathway
title_sort atorvastatin attenuates experimental contrast-induced acute kidney injury: a role for tlr4/myd88 signaling pathway
topic Laboratory Study
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6447912/
https://www.ncbi.nlm.nih.gov/pubmed/28805489
http://dx.doi.org/10.1080/0886022X.2017.1361838
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