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Protective effect of hydroxysafflor yellow A against acute kidney injury via the TLR4/NF-κB signaling pathway

This study aimed to evaluate the protective effect of hydroxysafflor yellow A (HSYA) on ischemia/reperfusion (I/R)-induced acute kidney injury via the TLR4/NF-κB pathway, both in vitro and in vivo. Rats were subjected to removal of the right kidney and I/R injury to the left kidney. Rats subjected t...

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Autores principales: Bai, Juan, Zhao, Jinyi, Cui, Dongxiao, Wang, Fan, Song, Ying, Cheng, Lianghua, Gao, Kai, Wang, Jin, Li, Long, Li, Shujun, Jia, Yanyan, Wen, Aidong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6003992/
https://www.ncbi.nlm.nih.gov/pubmed/29907783
http://dx.doi.org/10.1038/s41598-018-27217-3
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author Bai, Juan
Zhao, Jinyi
Cui, Dongxiao
Wang, Fan
Song, Ying
Cheng, Lianghua
Gao, Kai
Wang, Jin
Li, Long
Li, Shujun
Jia, Yanyan
Wen, Aidong
author_facet Bai, Juan
Zhao, Jinyi
Cui, Dongxiao
Wang, Fan
Song, Ying
Cheng, Lianghua
Gao, Kai
Wang, Jin
Li, Long
Li, Shujun
Jia, Yanyan
Wen, Aidong
author_sort Bai, Juan
collection PubMed
description This study aimed to evaluate the protective effect of hydroxysafflor yellow A (HSYA) on ischemia/reperfusion (I/R)-induced acute kidney injury via the TLR4/NF-κB pathway, both in vitro and in vivo. Rats were subjected to removal of the right kidney and I/R injury to the left kidney. Rats subjected to renal I/R injury were treated with HSYA at 0.5 h prior to I/R injury. Renal function, histopathological analysis, and cells apoptosis were measured in vivo. In vitro, proximal renal tubular cells (HK-2) were subjected to hypoxia/reoxygenation (H/R). Apoptotic cell death and inflammatory cytokines, Toll-like receptor 4 (TLR4), and nuclear factor (NF)-κB expression were determined. Treatment of I/R rats with HSYA markedly reduced the levels of serum creatinine and blood urea nitrogen, attenuated renal cell apoptosis, alleviated changes in renal tissue morphology, and reduced IL-1β, TNF-α, and caspase-3 release. In vitro, HSYA effectively decreased NF-κB p65 and inflammatory cytokines, such as IL-1β, TNF-α, and IL-6. Thus, HSYA can protect renal function from I/R injury by ameliorating acute kidney injury and partly by promoting tubular cell survival via the TLR4/NF-κB pathway. These results suggest that HSYA can be used to prevent I/R-induced acute kidney injury.
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spelling pubmed-60039922018-06-26 Protective effect of hydroxysafflor yellow A against acute kidney injury via the TLR4/NF-κB signaling pathway Bai, Juan Zhao, Jinyi Cui, Dongxiao Wang, Fan Song, Ying Cheng, Lianghua Gao, Kai Wang, Jin Li, Long Li, Shujun Jia, Yanyan Wen, Aidong Sci Rep Article This study aimed to evaluate the protective effect of hydroxysafflor yellow A (HSYA) on ischemia/reperfusion (I/R)-induced acute kidney injury via the TLR4/NF-κB pathway, both in vitro and in vivo. Rats were subjected to removal of the right kidney and I/R injury to the left kidney. Rats subjected to renal I/R injury were treated with HSYA at 0.5 h prior to I/R injury. Renal function, histopathological analysis, and cells apoptosis were measured in vivo. In vitro, proximal renal tubular cells (HK-2) were subjected to hypoxia/reoxygenation (H/R). Apoptotic cell death and inflammatory cytokines, Toll-like receptor 4 (TLR4), and nuclear factor (NF)-κB expression were determined. Treatment of I/R rats with HSYA markedly reduced the levels of serum creatinine and blood urea nitrogen, attenuated renal cell apoptosis, alleviated changes in renal tissue morphology, and reduced IL-1β, TNF-α, and caspase-3 release. In vitro, HSYA effectively decreased NF-κB p65 and inflammatory cytokines, such as IL-1β, TNF-α, and IL-6. Thus, HSYA can protect renal function from I/R injury by ameliorating acute kidney injury and partly by promoting tubular cell survival via the TLR4/NF-κB pathway. These results suggest that HSYA can be used to prevent I/R-induced acute kidney injury. Nature Publishing Group UK 2018-06-15 /pmc/articles/PMC6003992/ /pubmed/29907783 http://dx.doi.org/10.1038/s41598-018-27217-3 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Bai, Juan
Zhao, Jinyi
Cui, Dongxiao
Wang, Fan
Song, Ying
Cheng, Lianghua
Gao, Kai
Wang, Jin
Li, Long
Li, Shujun
Jia, Yanyan
Wen, Aidong
Protective effect of hydroxysafflor yellow A against acute kidney injury via the TLR4/NF-κB signaling pathway
title Protective effect of hydroxysafflor yellow A against acute kidney injury via the TLR4/NF-κB signaling pathway
title_full Protective effect of hydroxysafflor yellow A against acute kidney injury via the TLR4/NF-κB signaling pathway
title_fullStr Protective effect of hydroxysafflor yellow A against acute kidney injury via the TLR4/NF-κB signaling pathway
title_full_unstemmed Protective effect of hydroxysafflor yellow A against acute kidney injury via the TLR4/NF-κB signaling pathway
title_short Protective effect of hydroxysafflor yellow A against acute kidney injury via the TLR4/NF-κB signaling pathway
title_sort protective effect of hydroxysafflor yellow a against acute kidney injury via the tlr4/nf-κb signaling pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6003992/
https://www.ncbi.nlm.nih.gov/pubmed/29907783
http://dx.doi.org/10.1038/s41598-018-27217-3
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