Didymin, a natural flavonoid, relieves the progression of myocardial infarction via inhibiting the NLR family pyrin domain containing 3 inflammasome
Context Globally, the morbidity and mortality of cardiovascular diseases remain high. Didymin, a flavonoid glycoside, has long been used as a dietary antioxidant.Objective To determine the role of didymin in myocardial infarction (MI), and its possible myocardial protective mechanism.Materials and m...
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Taylor & Francis Group
2022-12-01
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Online Access: | https://www.tandfonline.com/doi/10.1080/13880209.2022.2148170 |
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author | Yong Zhang GuLi RuXian |
author_facet | Yong Zhang GuLi RuXian |
author_sort | Yong Zhang |
collection | DOAJ |
description | Context Globally, the morbidity and mortality of cardiovascular diseases remain high. Didymin, a flavonoid glycoside, has long been used as a dietary antioxidant.Objective To determine the role of didymin in myocardial infarction (MI), and its possible myocardial protective mechanism.Materials and methods C57/BL6 mice (aged 6–8 weeks, n = 40) were divided into five groups: sham group, ischaemia–reperfusion (I/R) group, I/R + didymin (1 mg/kg) group, I/R + didymin (2 mg/kg) group and I/R + didymin (4 mg/kg) group. Didymin was administered intragastrically daily before I/R for 5 consecutive days. H9C2 cells were divided into five groups: control group, H/R group, H/R + didymin (3 μM) group, H/R + didymin (10 μM) group and H/R + didymin (30 μM) group. H9C2 cells were treated with didymin for 24 h before hypoxia/reoxygenation (H/R).Results In vivo, didymin reduced the pathological damage and fibrosis of myocardial tissues, decreased the levels of lactate dehydrogenase, creatine kinase, connective tissue growth factor, collagen I and collagen III. Moreover, didymin reduced myocardial apoptosis, inhibited NLRP3, ASC and caspase-1 expression, and alleviated the inflammatory response. In vitro, didymin reduced MI, apoptosis, inflammation and the levels of NLRP3, ASC and caspase-1 in H9C2.Discussion and conclusions Didymin prevented the deterioration of MI by inhibiting NLRP3 inflammasome in vivo and in vitro, and may be a potential natural drug for the treatment of MI. Our study provides the scientific basis for further research of didymin. |
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language | English |
last_indexed | 2024-04-11T13:51:57Z |
publishDate | 2022-12-01 |
publisher | Taylor & Francis Group |
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series | Pharmaceutical Biology |
spelling | doaj.art-e9c390b7ff37403787192fb192e327e02022-12-22T04:20:35ZengTaylor & Francis GroupPharmaceutical Biology1388-02091744-51162022-12-016012319232710.1080/13880209.2022.2148170Didymin, a natural flavonoid, relieves the progression of myocardial infarction via inhibiting the NLR family pyrin domain containing 3 inflammasomeYong Zhang0GuLi RuXian1Department of Cardiology, First Affiliated Hospital, School of Medicine, Shihezi University, Shihezi, ChinaDepartment of Digestive Internal Medicine, School of Medicine, First Affiliated Hospital, Shihezi University, Shihezi, ChinaContext Globally, the morbidity and mortality of cardiovascular diseases remain high. Didymin, a flavonoid glycoside, has long been used as a dietary antioxidant.Objective To determine the role of didymin in myocardial infarction (MI), and its possible myocardial protective mechanism.Materials and methods C57/BL6 mice (aged 6–8 weeks, n = 40) were divided into five groups: sham group, ischaemia–reperfusion (I/R) group, I/R + didymin (1 mg/kg) group, I/R + didymin (2 mg/kg) group and I/R + didymin (4 mg/kg) group. Didymin was administered intragastrically daily before I/R for 5 consecutive days. H9C2 cells were divided into five groups: control group, H/R group, H/R + didymin (3 μM) group, H/R + didymin (10 μM) group and H/R + didymin (30 μM) group. H9C2 cells were treated with didymin for 24 h before hypoxia/reoxygenation (H/R).Results In vivo, didymin reduced the pathological damage and fibrosis of myocardial tissues, decreased the levels of lactate dehydrogenase, creatine kinase, connective tissue growth factor, collagen I and collagen III. Moreover, didymin reduced myocardial apoptosis, inhibited NLRP3, ASC and caspase-1 expression, and alleviated the inflammatory response. In vitro, didymin reduced MI, apoptosis, inflammation and the levels of NLRP3, ASC and caspase-1 in H9C2.Discussion and conclusions Didymin prevented the deterioration of MI by inhibiting NLRP3 inflammasome in vivo and in vitro, and may be a potential natural drug for the treatment of MI. Our study provides the scientific basis for further research of didymin.https://www.tandfonline.com/doi/10.1080/13880209.2022.2148170Ischaemia–reperfusionNOD-like receptor protein 3fibrosis |
spellingShingle | Yong Zhang GuLi RuXian Didymin, a natural flavonoid, relieves the progression of myocardial infarction via inhibiting the NLR family pyrin domain containing 3 inflammasome Pharmaceutical Biology Ischaemia–reperfusion NOD-like receptor protein 3 fibrosis |
title | Didymin, a natural flavonoid, relieves the progression of myocardial infarction via inhibiting the NLR family pyrin domain containing 3 inflammasome |
title_full | Didymin, a natural flavonoid, relieves the progression of myocardial infarction via inhibiting the NLR family pyrin domain containing 3 inflammasome |
title_fullStr | Didymin, a natural flavonoid, relieves the progression of myocardial infarction via inhibiting the NLR family pyrin domain containing 3 inflammasome |
title_full_unstemmed | Didymin, a natural flavonoid, relieves the progression of myocardial infarction via inhibiting the NLR family pyrin domain containing 3 inflammasome |
title_short | Didymin, a natural flavonoid, relieves the progression of myocardial infarction via inhibiting the NLR family pyrin domain containing 3 inflammasome |
title_sort | didymin a natural flavonoid relieves the progression of myocardial infarction via inhibiting the nlr family pyrin domain containing 3 inflammasome |
topic | Ischaemia–reperfusion NOD-like receptor protein 3 fibrosis |
url | https://www.tandfonline.com/doi/10.1080/13880209.2022.2148170 |
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