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Lycium barbarum polysaccharide attenuates cardiac hypertrophy, inhibits calpain-1 expression and inhibits NF-κB activation in streptozotocin-induced diabetic rats
Cardiac hypertrophy is one of the key structural changes that occurs in diabetic cardiomyopathy. Previous studies have indicated that the activation of NF-κB by calpain-1, a Ca(2+)-dependent cysteine protease, serves an important role in cardiac hypertrophy. The aim of the present study was to asses...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6566019/ https://www.ncbi.nlm.nih.gov/pubmed/31258688 http://dx.doi.org/10.3892/etm.2019.7612 |
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author | Liu, Qianqian Han, Qianqian Lu, Meili Wang, Hongxin Tang, Futian |
author_facet | Liu, Qianqian Han, Qianqian Lu, Meili Wang, Hongxin Tang, Futian |
author_sort | Liu, Qianqian |
collection | PubMed |
description | Cardiac hypertrophy is one of the key structural changes that occurs in diabetic cardiomyopathy. Previous studies have indicated that the activation of NF-κB by calpain-1, a Ca(2+)-dependent cysteine protease, serves an important role in cardiac hypertrophy. The aim of the present study was to assess the effect of 30 and 60 mg/kg Lycium barbarum polysaccharide (LBP) treatment, the major active ingredient extracted from Lycium barbarum, on cardiac hypertrophy in streptozotocin (STZ) induced diabetic rats. In addition, the present study examined the possible underlying mechanisms of this effect by assessing calpain-1 expression and the NF-κB pathway. The mRNA expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was determined by reverse transcription-quantitative PCR. Western blotting was used to detect the protein expressions of calpain-1, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and toll-like receptor-4 (TLR-4) in the heart tissue. The results revealed that compared with non-diabetic rats, diabetic rats exhibited cardiac hypertrophy. Cardiac hypertrophy was defined by the following: Dysfunction of the cardiac hemodynamics, an increase in the ratios of left ventricular weight/body weight and heart weight/body weight and the increased expressions of ANP and BNP, which serve as hypertrophic markers in cardiac tissue. However, all of these changes were attenuated in diabetic rats treated with LBP. In addition, the protein expression of calpain-1 was increased in the heart tissue of diabetic rats compared with that of non-diabetic rats, where it was inhibited by LBP. LBP also decreased the protein expression of certain inflammatory mediators, IL-6, TNF-α, ICAM-1, VCAM-1 and TLR-4 in diabetic heart tissue. Furthermore, LBP treatment reduced the production of reactive oxygen species, upregulated the protein expression of endothelial nitric oxide synthase and downregulated the protein expression of inducible nitric-oxide synthase. Additionally, LBP increased the protein expression of p65, the subunit of NF-κB and inhibitory protein кB-α in the cytoplasm and reduced p65 expression in the nucleus. In conclusion, LBP improves cardiac hypertrophy, inhibits the expression of calpain-1 and inhibits the activation of NF-κB in diabetic rats. |
format | Online Article Text |
id | pubmed-6566019 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-65660192019-06-28 Lycium barbarum polysaccharide attenuates cardiac hypertrophy, inhibits calpain-1 expression and inhibits NF-κB activation in streptozotocin-induced diabetic rats Liu, Qianqian Han, Qianqian Lu, Meili Wang, Hongxin Tang, Futian Exp Ther Med Articles Cardiac hypertrophy is one of the key structural changes that occurs in diabetic cardiomyopathy. Previous studies have indicated that the activation of NF-κB by calpain-1, a Ca(2+)-dependent cysteine protease, serves an important role in cardiac hypertrophy. The aim of the present study was to assess the effect of 30 and 60 mg/kg Lycium barbarum polysaccharide (LBP) treatment, the major active ingredient extracted from Lycium barbarum, on cardiac hypertrophy in streptozotocin (STZ) induced diabetic rats. In addition, the present study examined the possible underlying mechanisms of this effect by assessing calpain-1 expression and the NF-κB pathway. The mRNA expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was determined by reverse transcription-quantitative PCR. Western blotting was used to detect the protein expressions of calpain-1, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1) and toll-like receptor-4 (TLR-4) in the heart tissue. The results revealed that compared with non-diabetic rats, diabetic rats exhibited cardiac hypertrophy. Cardiac hypertrophy was defined by the following: Dysfunction of the cardiac hemodynamics, an increase in the ratios of left ventricular weight/body weight and heart weight/body weight and the increased expressions of ANP and BNP, which serve as hypertrophic markers in cardiac tissue. However, all of these changes were attenuated in diabetic rats treated with LBP. In addition, the protein expression of calpain-1 was increased in the heart tissue of diabetic rats compared with that of non-diabetic rats, where it was inhibited by LBP. LBP also decreased the protein expression of certain inflammatory mediators, IL-6, TNF-α, ICAM-1, VCAM-1 and TLR-4 in diabetic heart tissue. Furthermore, LBP treatment reduced the production of reactive oxygen species, upregulated the protein expression of endothelial nitric oxide synthase and downregulated the protein expression of inducible nitric-oxide synthase. Additionally, LBP increased the protein expression of p65, the subunit of NF-κB and inhibitory protein кB-α in the cytoplasm and reduced p65 expression in the nucleus. In conclusion, LBP improves cardiac hypertrophy, inhibits the expression of calpain-1 and inhibits the activation of NF-κB in diabetic rats. D.A. Spandidos 2019-07 2019-05-24 /pmc/articles/PMC6566019/ /pubmed/31258688 http://dx.doi.org/10.3892/etm.2019.7612 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, Qianqian Han, Qianqian Lu, Meili Wang, Hongxin Tang, Futian Lycium barbarum polysaccharide attenuates cardiac hypertrophy, inhibits calpain-1 expression and inhibits NF-κB activation in streptozotocin-induced diabetic rats |
title | Lycium barbarum polysaccharide attenuates cardiac hypertrophy, inhibits calpain-1 expression and inhibits NF-κB activation in streptozotocin-induced diabetic rats |
title_full | Lycium barbarum polysaccharide attenuates cardiac hypertrophy, inhibits calpain-1 expression and inhibits NF-κB activation in streptozotocin-induced diabetic rats |
title_fullStr | Lycium barbarum polysaccharide attenuates cardiac hypertrophy, inhibits calpain-1 expression and inhibits NF-κB activation in streptozotocin-induced diabetic rats |
title_full_unstemmed | Lycium barbarum polysaccharide attenuates cardiac hypertrophy, inhibits calpain-1 expression and inhibits NF-κB activation in streptozotocin-induced diabetic rats |
title_short | Lycium barbarum polysaccharide attenuates cardiac hypertrophy, inhibits calpain-1 expression and inhibits NF-κB activation in streptozotocin-induced diabetic rats |
title_sort | lycium barbarum polysaccharide attenuates cardiac hypertrophy, inhibits calpain-1 expression and inhibits nf-κb activation in streptozotocin-induced diabetic rats |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6566019/ https://www.ncbi.nlm.nih.gov/pubmed/31258688 http://dx.doi.org/10.3892/etm.2019.7612 |
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