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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Main Authors: Yong Zhang, GuLi RuXian
Format: Article
Language:English
Published: Taylor & Francis Group 2022-12-01
Series:Pharmaceutical Biology
Subjects:
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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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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