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Protective effect of Guanxin Danshen formula on myocardial ischemiareperfusion injury in rats
PURPOSE: Myocardial ischemia/reperfusion injury (MIRI) leads to myocardial tissue necrosis, which will increase the size of myocardial infarction. The study examined the protective effect and mechanism of the Guanxin Danshen formula (GXDSF) on MIRI in rats. METHODS: MIRI model was performed in rats;...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10129295/ https://www.ncbi.nlm.nih.gov/pubmed/37098925 http://dx.doi.org/10.1590/acb380123 |
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author | Li, Lanfang Liu, Bo Wang, Min Ye, Jingxue Sun, Guibo |
author_facet | Li, Lanfang Liu, Bo Wang, Min Ye, Jingxue Sun, Guibo |
author_sort | Li, Lanfang |
collection | PubMed |
description | PURPOSE: Myocardial ischemia/reperfusion injury (MIRI) leads to myocardial tissue necrosis, which will increase the size of myocardial infarction. The study examined the protective effect and mechanism of the Guanxin Danshen formula (GXDSF) on MIRI in rats. METHODS: MIRI model was performed in rats; rat H9C2 cardiomyocytes were hypoxia-reoxygenated to establish a cell injury model. RESULTS: The GXDSF significantly reduced myocardial ischemia area, reduced myocardial structural injury, decreased the levels of interleukin (IL-1β, IL-6) in serum, decreased the activity of myocardial enzymes, increased the activity of superoxide dismutase (SOD), and reduced glutathione in rats with MIRI. The GXDSF can reduce the expression of nucleotide- binding oligomerization domain, leucine-rich repeat and pyrin domain containing nod-like receptor family protein 3 (NLRP3), IL-1β, caspase-1, and gasdermin D (GSDMD) in myocardial tissue cells. Salvianolic acid B and notoginsenoside R1 protected H9C2 cardiomyocytes from hypoxia and reoxygenation injury and reduced the levels of tumor necrosis factor α (TNF-α) and IL-6 in the cell supernatant, decreasing the NLRP3, IL-18, IL-1β, caspase-1, and GSDMD expression in H9C2 cardiomyocytes. GXDSF can reduce the myocardial infarction area and alleviate the damage to myocardial structure in rats with MIRI, which may be related to the regulation of the NLRP3. CONCLUSIONS: GXDSF reduces MIRI in rat myocardial infarction injury, improves structural damage in myocardial ischemia injury, and reduces myocardial tissue inflammation and oxidative stress by lowering inflammatory factors and controlling focal cell death signaling pathways. |
format | Online Article Text |
id | pubmed-10129295 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia |
record_format | MEDLINE/PubMed |
spelling | pubmed-101292952023-04-26 Protective effect of Guanxin Danshen formula on myocardial ischemiareperfusion injury in rats Li, Lanfang Liu, Bo Wang, Min Ye, Jingxue Sun, Guibo Acta Cir Bras Original Article PURPOSE: Myocardial ischemia/reperfusion injury (MIRI) leads to myocardial tissue necrosis, which will increase the size of myocardial infarction. The study examined the protective effect and mechanism of the Guanxin Danshen formula (GXDSF) on MIRI in rats. METHODS: MIRI model was performed in rats; rat H9C2 cardiomyocytes were hypoxia-reoxygenated to establish a cell injury model. RESULTS: The GXDSF significantly reduced myocardial ischemia area, reduced myocardial structural injury, decreased the levels of interleukin (IL-1β, IL-6) in serum, decreased the activity of myocardial enzymes, increased the activity of superoxide dismutase (SOD), and reduced glutathione in rats with MIRI. The GXDSF can reduce the expression of nucleotide- binding oligomerization domain, leucine-rich repeat and pyrin domain containing nod-like receptor family protein 3 (NLRP3), IL-1β, caspase-1, and gasdermin D (GSDMD) in myocardial tissue cells. Salvianolic acid B and notoginsenoside R1 protected H9C2 cardiomyocytes from hypoxia and reoxygenation injury and reduced the levels of tumor necrosis factor α (TNF-α) and IL-6 in the cell supernatant, decreasing the NLRP3, IL-18, IL-1β, caspase-1, and GSDMD expression in H9C2 cardiomyocytes. GXDSF can reduce the myocardial infarction area and alleviate the damage to myocardial structure in rats with MIRI, which may be related to the regulation of the NLRP3. CONCLUSIONS: GXDSF reduces MIRI in rat myocardial infarction injury, improves structural damage in myocardial ischemia injury, and reduces myocardial tissue inflammation and oxidative stress by lowering inflammatory factors and controlling focal cell death signaling pathways. Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia 2023-04-21 /pmc/articles/PMC10129295/ /pubmed/37098925 http://dx.doi.org/10.1590/acb380123 Text en https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Li, Lanfang Liu, Bo Wang, Min Ye, Jingxue Sun, Guibo Protective effect of Guanxin Danshen formula on myocardial ischemiareperfusion injury in rats |
title | Protective effect of Guanxin Danshen formula on myocardial ischemiareperfusion injury in rats |
title_full | Protective effect of Guanxin Danshen formula on myocardial ischemiareperfusion injury in rats |
title_fullStr | Protective effect of Guanxin Danshen formula on myocardial ischemiareperfusion injury in rats |
title_full_unstemmed | Protective effect of Guanxin Danshen formula on myocardial ischemiareperfusion injury in rats |
title_short | Protective effect of Guanxin Danshen formula on myocardial ischemiareperfusion injury in rats |
title_sort | protective effect of guanxin danshen formula on myocardial ischemiareperfusion injury in rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10129295/ https://www.ncbi.nlm.nih.gov/pubmed/37098925 http://dx.doi.org/10.1590/acb380123 |
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