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Gandouling Mitigates CuSO(4)-Induced Heart Injury in Rats

SIMPLE SUMMARY: Wilson’s disease (WD) is a rare autosomal recessive inherited disorder of copper (Cu) metabolism, which is one of the few neurogenetic diseases with a cure. Cu deposition in the heart tissue is a mechanism of cardiac involvement. Importantly, Gandouling (GDL) effectively promotes the...

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Autores principales: Fang, Shuzhen, Yang, Wenming, Zhang, Kangyi, Peng, Chuanyi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9559265/
https://www.ncbi.nlm.nih.gov/pubmed/36230444
http://dx.doi.org/10.3390/ani12192703
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author Fang, Shuzhen
Yang, Wenming
Zhang, Kangyi
Peng, Chuanyi
author_facet Fang, Shuzhen
Yang, Wenming
Zhang, Kangyi
Peng, Chuanyi
author_sort Fang, Shuzhen
collection PubMed
description SIMPLE SUMMARY: Wilson’s disease (WD) is a rare autosomal recessive inherited disorder of copper (Cu) metabolism, which is one of the few neurogenetic diseases with a cure. Cu deposition in the heart tissue is a mechanism of cardiac involvement. Importantly, Gandouling (GDL) effectively promotes the excretion of intracellular Cu. Therefore, the purpose of this study was to evaluate the protective effects of GDL on heart injuries and the underlying mechanisms in a copper sulfate (CuSO4)-induced animal model. The results showed that the protective effect of GDL on the heart was superior to that of penicillamine. ABSTRACT: We assessed the protective effects of Gandouling (GDL) on copper sulfate (CuSO(4))-induced heart injuries in Sprague–Dawley rats, which were randomly divided into the control, CuSO(4), GDL + CuSO(4) and penicillamine + CuSO(4) groups. The rats received intragastric GDL (400 mg/kg body weight) once per day for 42 consecutive days after 56 days of CuSO(4) exposure, and penicillamine was used as a positive control. The levels of plasma inflammatory cytokines (IMA, hFABP, cTn-I and BNP) were determined using the enzyme-linked immunosorbent assay. The histopathological symptoms were evaluated using hematoxylin and eosin staining and transmission electron microscopy. To determine the underlying mechanism, Western blotting was conducted for the detection of the heme oxygenase 1 (HO-1) expression. The results revealed that GDL supplementation alleviated the histopathological symptoms of the rat heart tissue, promoted Cu excretion to attenuate impairment, and significantly decreased inflammatory cytokine levels in the plasma (p < 0.01). In addition, GDL increased the HO-1 expression in the rat hepatic tissue. The protective effect of GDL on the heart was superior to that of penicillamine. Overall, these findings indicate that GDL alleviates hepatic heart injury after a Cu overaccumulation challenge, and GDL supplements can be beneficial for patients with Wilson’s disease.
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spelling pubmed-95592652022-10-14 Gandouling Mitigates CuSO(4)-Induced Heart Injury in Rats Fang, Shuzhen Yang, Wenming Zhang, Kangyi Peng, Chuanyi Animals (Basel) Article SIMPLE SUMMARY: Wilson’s disease (WD) is a rare autosomal recessive inherited disorder of copper (Cu) metabolism, which is one of the few neurogenetic diseases with a cure. Cu deposition in the heart tissue is a mechanism of cardiac involvement. Importantly, Gandouling (GDL) effectively promotes the excretion of intracellular Cu. Therefore, the purpose of this study was to evaluate the protective effects of GDL on heart injuries and the underlying mechanisms in a copper sulfate (CuSO4)-induced animal model. The results showed that the protective effect of GDL on the heart was superior to that of penicillamine. ABSTRACT: We assessed the protective effects of Gandouling (GDL) on copper sulfate (CuSO(4))-induced heart injuries in Sprague–Dawley rats, which were randomly divided into the control, CuSO(4), GDL + CuSO(4) and penicillamine + CuSO(4) groups. The rats received intragastric GDL (400 mg/kg body weight) once per day for 42 consecutive days after 56 days of CuSO(4) exposure, and penicillamine was used as a positive control. The levels of plasma inflammatory cytokines (IMA, hFABP, cTn-I and BNP) were determined using the enzyme-linked immunosorbent assay. The histopathological symptoms were evaluated using hematoxylin and eosin staining and transmission electron microscopy. To determine the underlying mechanism, Western blotting was conducted for the detection of the heme oxygenase 1 (HO-1) expression. The results revealed that GDL supplementation alleviated the histopathological symptoms of the rat heart tissue, promoted Cu excretion to attenuate impairment, and significantly decreased inflammatory cytokine levels in the plasma (p < 0.01). In addition, GDL increased the HO-1 expression in the rat hepatic tissue. The protective effect of GDL on the heart was superior to that of penicillamine. Overall, these findings indicate that GDL alleviates hepatic heart injury after a Cu overaccumulation challenge, and GDL supplements can be beneficial for patients with Wilson’s disease. MDPI 2022-10-08 /pmc/articles/PMC9559265/ /pubmed/36230444 http://dx.doi.org/10.3390/ani12192703 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Fang, Shuzhen
Yang, Wenming
Zhang, Kangyi
Peng, Chuanyi
Gandouling Mitigates CuSO(4)-Induced Heart Injury in Rats
title Gandouling Mitigates CuSO(4)-Induced Heart Injury in Rats
title_full Gandouling Mitigates CuSO(4)-Induced Heart Injury in Rats
title_fullStr Gandouling Mitigates CuSO(4)-Induced Heart Injury in Rats
title_full_unstemmed Gandouling Mitigates CuSO(4)-Induced Heart Injury in Rats
title_short Gandouling Mitigates CuSO(4)-Induced Heart Injury in Rats
title_sort gandouling mitigates cuso(4)-induced heart injury in rats
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9559265/
https://www.ncbi.nlm.nih.gov/pubmed/36230444
http://dx.doi.org/10.3390/ani12192703
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