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Luteolin attenuates angiotensin II-induced renal damage in apolipoprotein E-deficient mice

Renal damage is a common and severe condition encountered in the clinic. Luteolin (Lut) exhibits anti-inflammatory, anti-fibrotic and anti-apoptotic effects. Thus, the present study aimed to investigate the pharmacological effects of Lut on angiotensin II (AngII)-induced renal damage in apolipoprote...

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Autores principales: Liu, Ying-Shu, Yang, Qin, Li, Shen, Luo, Lan, Liu, Hong-Yang, Li, Xin-Yu, Gao, Zheng-Nan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7789115/
https://www.ncbi.nlm.nih.gov/pubmed/33355379
http://dx.doi.org/10.3892/mmr.2020.11796
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author Liu, Ying-Shu
Yang, Qin
Li, Shen
Luo, Lan
Liu, Hong-Yang
Li, Xin-Yu
Gao, Zheng-Nan
author_facet Liu, Ying-Shu
Yang, Qin
Li, Shen
Luo, Lan
Liu, Hong-Yang
Li, Xin-Yu
Gao, Zheng-Nan
author_sort Liu, Ying-Shu
collection PubMed
description Renal damage is a common and severe condition encountered in the clinic. Luteolin (Lut) exhibits anti-inflammatory, anti-fibrotic and anti-apoptotic effects. Thus, the present study aimed to investigate the pharmacological effects of Lut on angiotensin II (AngII)-induced renal damage in apolipoprotein E-deficient (ApoE(−/−)) mice. Male ApoE(−/−) mice (age, 8 weeks) were randomly divided into the following three groups: i) Control group (n=6); ii) AngII group (n=6); and iii) AngII + Lut group (n=6). Lut was administered by gavage (100 mg/kg/d). ApoE(−/−) mice were implanted with Alzet osmotic minipumps, filled with either saline vehicle or AngII solution for a maximum period of 4 weeks. After 4 weeks, metabolic characteristics were measured and the histopathological alterations in the kidney tissue were observed. The metabolic characteristics of blood creatinine (CRE) levels were lower in the AngII + Lut group compared with in the AngII group. The expression levels of collagen I and III were lower in the kidney tissues of the AngII + Lut group compared with the corresponding tissues of the AngII group. The gene expression levels of IL-1β, IL-6, TNF-α and IL-10 were also suppressed in the kidney tissues of the AngII + Lut group compared with those in the corresponding tissues of the AngII group. Furthermore, the AngII + Lut group exhibited markedly increased LC3 protein expression and notably decreased p62 protein expression in the kidney tissues compared with the expression levels in the AngII group. The data demonstrated that Lut attenuated AngII-induced collagen deposition and inflammation, while inducing autophagy. Collectively, the results suggested that Lut treatment exhibited a exerted effect on AngII-induced renal injury in ApoE(−/−) mice.
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spelling pubmed-77891152021-01-11 Luteolin attenuates angiotensin II-induced renal damage in apolipoprotein E-deficient mice Liu, Ying-Shu Yang, Qin Li, Shen Luo, Lan Liu, Hong-Yang Li, Xin-Yu Gao, Zheng-Nan Mol Med Rep Articles Renal damage is a common and severe condition encountered in the clinic. Luteolin (Lut) exhibits anti-inflammatory, anti-fibrotic and anti-apoptotic effects. Thus, the present study aimed to investigate the pharmacological effects of Lut on angiotensin II (AngII)-induced renal damage in apolipoprotein E-deficient (ApoE(−/−)) mice. Male ApoE(−/−) mice (age, 8 weeks) were randomly divided into the following three groups: i) Control group (n=6); ii) AngII group (n=6); and iii) AngII + Lut group (n=6). Lut was administered by gavage (100 mg/kg/d). ApoE(−/−) mice were implanted with Alzet osmotic minipumps, filled with either saline vehicle or AngII solution for a maximum period of 4 weeks. After 4 weeks, metabolic characteristics were measured and the histopathological alterations in the kidney tissue were observed. The metabolic characteristics of blood creatinine (CRE) levels were lower in the AngII + Lut group compared with in the AngII group. The expression levels of collagen I and III were lower in the kidney tissues of the AngII + Lut group compared with the corresponding tissues of the AngII group. The gene expression levels of IL-1β, IL-6, TNF-α and IL-10 were also suppressed in the kidney tissues of the AngII + Lut group compared with those in the corresponding tissues of the AngII group. Furthermore, the AngII + Lut group exhibited markedly increased LC3 protein expression and notably decreased p62 protein expression in the kidney tissues compared with the expression levels in the AngII group. The data demonstrated that Lut attenuated AngII-induced collagen deposition and inflammation, while inducing autophagy. Collectively, the results suggested that Lut treatment exhibited a exerted effect on AngII-induced renal injury in ApoE(−/−) mice. D.A. Spandidos 2021-02 2020-12-22 /pmc/articles/PMC7789115/ /pubmed/33355379 http://dx.doi.org/10.3892/mmr.2020.11796 Text en Copyright: © Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Liu, Ying-Shu
Yang, Qin
Li, Shen
Luo, Lan
Liu, Hong-Yang
Li, Xin-Yu
Gao, Zheng-Nan
Luteolin attenuates angiotensin II-induced renal damage in apolipoprotein E-deficient mice
title Luteolin attenuates angiotensin II-induced renal damage in apolipoprotein E-deficient mice
title_full Luteolin attenuates angiotensin II-induced renal damage in apolipoprotein E-deficient mice
title_fullStr Luteolin attenuates angiotensin II-induced renal damage in apolipoprotein E-deficient mice
title_full_unstemmed Luteolin attenuates angiotensin II-induced renal damage in apolipoprotein E-deficient mice
title_short Luteolin attenuates angiotensin II-induced renal damage in apolipoprotein E-deficient mice
title_sort luteolin attenuates angiotensin ii-induced renal damage in apolipoprotein e-deficient mice
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7789115/
https://www.ncbi.nlm.nih.gov/pubmed/33355379
http://dx.doi.org/10.3892/mmr.2020.11796
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