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Ginkgo suppresses atherosclerosis through downregulating the expression of connexin 43 in rabbits
INTRODUCTION: Ginkgo biloba extract (GBE) EGb761 is widely used for cardiovascular prevention. Here, we investigated the effects of GBE on atherosclerotic lesion development in rabbits with a high-fat diet. MATERIAL AND METHODS: Forty New Zealand white male rabbits were randomly divided into four gr...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Termedia Publishing House
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648825/ https://www.ncbi.nlm.nih.gov/pubmed/23671447 http://dx.doi.org/10.5114/aoms.2013.34416 |
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author | Wei, Jian Ming Wang, Xin Gong, Hui Shi, Yi Jun Zou, Yunzeng |
author_facet | Wei, Jian Ming Wang, Xin Gong, Hui Shi, Yi Jun Zou, Yunzeng |
author_sort | Wei, Jian Ming |
collection | PubMed |
description | INTRODUCTION: Ginkgo biloba extract (GBE) EGb761 is widely used for cardiovascular prevention. Here, we investigated the effects of GBE on atherosclerotic lesion development in rabbits with a high-fat diet. MATERIAL AND METHODS: Forty New Zealand white male rabbits were randomly divided into four groups. The first two were the normal diet group (C) and the high-fat group (HF). The remaining two groups were those who received a high cholesterol diet supplemented with either the standard drug (simvastatin 2 mg/kg/day) or GBE (3 mg/kg/day). At 12 weeks, histopathological and chemical analyses were performed. RESULTS: Plasma lipid measurement showed that GBE inhibited high-fat diet-induced increase of serum triglyceride (TG), total cholesterol (TC), and low density lipoprotein cholesterol (LDL-C) by 59.1% (0.9 ±0.2 4 mmol/l vs. 2.2 ±0.4 mmol/l), 18.2% (31.1 ±1.4 mmol/l vs. 38.0 ±0.4 mmol/l) and 15% (28.9 ±1.3 mmol/l vs. 34.0±1.0 mmol/l), respectively, at 12 weeks (p < 0.01). The en face Sudan IV-positive lesion area of the aorta in the GBE group (51.7 ±3.1%) was significantly lower compared with that in the HF group (88.2 ±2.2%; p < 0.01). The mean atherosclerotic lesion area of the GBE group was reduced by 53.2% compared with the HF group (p < 0.01). Immunohistochemistry and western blot analysis showed that GBE markedly suppressed high-fat diet-induced upregulation of connexin 43 (Cx43) in rabbits (p < 0.01). CONCLUSIONS: Thus, our study revealed that GBE prevented atherosclerosis progress through modulating plasma lipid, suppressing atherosclerotic lesion development, and attenuating the expression of Cx43 protein. |
format | Online Article Text |
id | pubmed-3648825 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Termedia Publishing House |
record_format | MEDLINE/PubMed |
spelling | pubmed-36488252013-05-13 Ginkgo suppresses atherosclerosis through downregulating the expression of connexin 43 in rabbits Wei, Jian Ming Wang, Xin Gong, Hui Shi, Yi Jun Zou, Yunzeng Arch Med Sci Experimental Research INTRODUCTION: Ginkgo biloba extract (GBE) EGb761 is widely used for cardiovascular prevention. Here, we investigated the effects of GBE on atherosclerotic lesion development in rabbits with a high-fat diet. MATERIAL AND METHODS: Forty New Zealand white male rabbits were randomly divided into four groups. The first two were the normal diet group (C) and the high-fat group (HF). The remaining two groups were those who received a high cholesterol diet supplemented with either the standard drug (simvastatin 2 mg/kg/day) or GBE (3 mg/kg/day). At 12 weeks, histopathological and chemical analyses were performed. RESULTS: Plasma lipid measurement showed that GBE inhibited high-fat diet-induced increase of serum triglyceride (TG), total cholesterol (TC), and low density lipoprotein cholesterol (LDL-C) by 59.1% (0.9 ±0.2 4 mmol/l vs. 2.2 ±0.4 mmol/l), 18.2% (31.1 ±1.4 mmol/l vs. 38.0 ±0.4 mmol/l) and 15% (28.9 ±1.3 mmol/l vs. 34.0±1.0 mmol/l), respectively, at 12 weeks (p < 0.01). The en face Sudan IV-positive lesion area of the aorta in the GBE group (51.7 ±3.1%) was significantly lower compared with that in the HF group (88.2 ±2.2%; p < 0.01). The mean atherosclerotic lesion area of the GBE group was reduced by 53.2% compared with the HF group (p < 0.01). Immunohistochemistry and western blot analysis showed that GBE markedly suppressed high-fat diet-induced upregulation of connexin 43 (Cx43) in rabbits (p < 0.01). CONCLUSIONS: Thus, our study revealed that GBE prevented atherosclerosis progress through modulating plasma lipid, suppressing atherosclerotic lesion development, and attenuating the expression of Cx43 protein. Termedia Publishing House 2013-04-09 2013-04-20 /pmc/articles/PMC3648825/ /pubmed/23671447 http://dx.doi.org/10.5114/aoms.2013.34416 Text en Copyright © 2013 Termedia & Banach http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Experimental Research Wei, Jian Ming Wang, Xin Gong, Hui Shi, Yi Jun Zou, Yunzeng Ginkgo suppresses atherosclerosis through downregulating the expression of connexin 43 in rabbits |
title | Ginkgo suppresses atherosclerosis through downregulating the expression of connexin 43 in rabbits |
title_full | Ginkgo suppresses atherosclerosis through downregulating the expression of connexin 43 in rabbits |
title_fullStr | Ginkgo suppresses atherosclerosis through downregulating the expression of connexin 43 in rabbits |
title_full_unstemmed | Ginkgo suppresses atherosclerosis through downregulating the expression of connexin 43 in rabbits |
title_short | Ginkgo suppresses atherosclerosis through downregulating the expression of connexin 43 in rabbits |
title_sort | ginkgo suppresses atherosclerosis through downregulating the expression of connexin 43 in rabbits |
topic | Experimental Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648825/ https://www.ncbi.nlm.nih.gov/pubmed/23671447 http://dx.doi.org/10.5114/aoms.2013.34416 |
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