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Inhibition of vascular remodelling in a porcine coronary injury model by herbal extract XS0601

BACKGROUND: Arterial remodelling is a major pathologic change of restenosis after percutaneous coronary intervention (PCI). Our previous studies showed that XS0601 (consisting of Chuangxingol and paeoniflorin) had some effects on the prevention of restenosis after PCI. Therefore, the purpose of this...

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Autores principales: Xu, Hao, Shi, Dazhuo, Chen, Keji
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1761146/
https://www.ncbi.nlm.nih.gov/pubmed/17302965
http://dx.doi.org/10.1186/1749-8546-1-2
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author Xu, Hao
Shi, Dazhuo
Chen, Keji
author_facet Xu, Hao
Shi, Dazhuo
Chen, Keji
author_sort Xu, Hao
collection PubMed
description BACKGROUND: Arterial remodelling is a major pathologic change of restenosis after percutaneous coronary intervention (PCI). Our previous studies showed that XS0601 (consisting of Chuangxingol and paeoniflorin) had some effects on the prevention of restenosis after PCI. Therefore, the purpose of this study was to examine whether and how its mechanism was related to the regulation of the arterial remodelling after endothelial injury by balloon dilation. METHODS: Twenty Chinese mini-pigs were randomized into four groups: control, probucol, low-dose XS0601 and high-dose XS0601 group before oversized balloon injury of the left anterior descending coronary arteries. Starting from two days before balloon injury, the mini-pigs in the treated group were administered with probucol (2 g/day) and XS0601 (0.02 g/kg/day for low dose; 0.04 g/kg/day for high dose) for four weeks after balloon injury. The animals receiving balloon injury alone were used as control. Morphometric and angiographic analysis of the injured arteries were performed. RESULTS: The contribution of intimal hyperplasia and arterial remodelling to angiographic late lumen loss was 41% and 59% respectively. XS0601 markedly inhibited proliferation of smooth muscle cells (SMCs) and transformation of SMCs from contractile to synthetic phenotype in neointima, inhibited hyperplasia-related indices of morphometric analysis and reduce late angiographic lumen loss. The reduction of the late angiographic lumen loss resulting from vascular remodelling was greater after XS0601 treatment. CONCLUSION: Both intimal hyperplasia and vascular remodelling are attributed to late lumen loss in this porcine coronary injury model. XS0601 markedly reduced angiographic late lumen loss resulting from intimal hyperplasia, vascular remodelling and XS0601 may be a potential agent to prevent restenosis after PCI.
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spelling pubmed-17611462007-01-08 Inhibition of vascular remodelling in a porcine coronary injury model by herbal extract XS0601 Xu, Hao Shi, Dazhuo Chen, Keji Chin Med Research BACKGROUND: Arterial remodelling is a major pathologic change of restenosis after percutaneous coronary intervention (PCI). Our previous studies showed that XS0601 (consisting of Chuangxingol and paeoniflorin) had some effects on the prevention of restenosis after PCI. Therefore, the purpose of this study was to examine whether and how its mechanism was related to the regulation of the arterial remodelling after endothelial injury by balloon dilation. METHODS: Twenty Chinese mini-pigs were randomized into four groups: control, probucol, low-dose XS0601 and high-dose XS0601 group before oversized balloon injury of the left anterior descending coronary arteries. Starting from two days before balloon injury, the mini-pigs in the treated group were administered with probucol (2 g/day) and XS0601 (0.02 g/kg/day for low dose; 0.04 g/kg/day for high dose) for four weeks after balloon injury. The animals receiving balloon injury alone were used as control. Morphometric and angiographic analysis of the injured arteries were performed. RESULTS: The contribution of intimal hyperplasia and arterial remodelling to angiographic late lumen loss was 41% and 59% respectively. XS0601 markedly inhibited proliferation of smooth muscle cells (SMCs) and transformation of SMCs from contractile to synthetic phenotype in neointima, inhibited hyperplasia-related indices of morphometric analysis and reduce late angiographic lumen loss. The reduction of the late angiographic lumen loss resulting from vascular remodelling was greater after XS0601 treatment. CONCLUSION: Both intimal hyperplasia and vascular remodelling are attributed to late lumen loss in this porcine coronary injury model. XS0601 markedly reduced angiographic late lumen loss resulting from intimal hyperplasia, vascular remodelling and XS0601 may be a potential agent to prevent restenosis after PCI. BioMed Central 2006-11-23 /pmc/articles/PMC1761146/ /pubmed/17302965 http://dx.doi.org/10.1186/1749-8546-1-2 Text en Copyright © 2006 Xu et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Xu, Hao
Shi, Dazhuo
Chen, Keji
Inhibition of vascular remodelling in a porcine coronary injury model by herbal extract XS0601
title Inhibition of vascular remodelling in a porcine coronary injury model by herbal extract XS0601
title_full Inhibition of vascular remodelling in a porcine coronary injury model by herbal extract XS0601
title_fullStr Inhibition of vascular remodelling in a porcine coronary injury model by herbal extract XS0601
title_full_unstemmed Inhibition of vascular remodelling in a porcine coronary injury model by herbal extract XS0601
title_short Inhibition of vascular remodelling in a porcine coronary injury model by herbal extract XS0601
title_sort inhibition of vascular remodelling in a porcine coronary injury model by herbal extract xs0601
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1761146/
https://www.ncbi.nlm.nih.gov/pubmed/17302965
http://dx.doi.org/10.1186/1749-8546-1-2
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