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.
Keywords: Ischaemia–reperfusion; NOD-like receptor protein 3; fibrosis.