Abstract
Purpose:Myocardial ischemia/reperfusion (Ml/R) injury is a leading cause of damage in cardiac tissues, with high rates of mortality and disability. Biochanin A (BCA) is a main constituent of Trifolium pratense L. This study was intended to explore the effect of BCA on Ml/R injury and explore the potential mechanism.Methods: In vivo MI/R injury was established by transient coronary ligation in Sprague-Dawley rats. Triphenyltetrazolium chloride staining (TTC) was used to measure myocardial infarct size. ELISA assay was employed to evaluate the levels of myocardial enzyme and inflammatory cytokines. Western blot assay was conducted to detect related protein levels in myocardial tissues.Results:BCA significantly ameliorated myocardial infarction area, reduced the release of myocardial enzyme levels including aspartate transaminase (AST), creatine kinase (CK-MB) and lactic dehydrogenase (LDH). It also decreased the production of inflammatory cytokines (IL-1β, IL-18, IL-6 and TNF-α) in serum of Ml/R rats. Further mechanism studies demonstrated that BCA inhibited inflammatory reaction through blocking TLR4/NF-kB/NLRP3 signaling pathway.Conclusion:The present study is the first evidence demonstrating that BCA attenuated Ml/R injury through suppressing TLR4/NF-kB/NLRP3 signaling pathway-mediated anti-inflammation pathway.
Highlights
Myocardial ischemia-reperfusion (MI/R) injury refers to the aggravation of myocardial tissue injury or even permanent irreversible injury after blood flow is resupplied due to myocardial ischemia injury[1]
The results from Triphenyltetrazolium chloride staining (TTC) staining revealed that the infarct area in I/R group was increased sharply as compared to that in the sham group, confirming the successful construction of rat model of MI/R (p
Biochanin A (BCA) (12.5, 25 and 50 mg/kg) observably reversed the abnormal increased infarct size in rats subjected to MI/R injury in a dose-dependent manner (p
Summary
Myocardial ischemia-reperfusion (MI/R) injury refers to the aggravation of myocardial tissue injury or even permanent irreversible injury after blood flow is resupplied due to myocardial ischemia injury[1]. It has become one of the cardiovascular diseases with the highest morbidity and mortality in developed and developing countries[2]. Basic studies have found that the pathological mechanism of MI/R is aerobic free radical injury, intracellular pH change, calcium overload, inflammatory factor infiltration, etc. Other factors include immune imbalance, endoplasmic reticulum stress, apoptosis and autophagy, myocardial energy metabolism disorder, myocardial microvascular endothelial cell injury and so on
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