Background
Sepsis is a systemic inflammatory disease, and Brevilin A (BA) has a powerful anti-inflammatory effect. However, whether BA has a similar effect on septic cardiomyopathy remains unclear. This study aimed to investigate the effect and mechanism of BA in septic cardiomyopathy.
Conclusion
BA ameliorated sepsis cardiomyopathy by inhibiting NF-κB/NLRP3 inflammation activation.
Methods
First, a model of septic cardiomyopathy was constructed in vitro and in vivo. The expression of the cardiac injury markers, NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammation factors and its upstream modulator NF-κB was detected by real-time polymerase chain reaction and western blotting. Cardiac function was measured using echocardiography, cell viability was detected using the methyl thiazolyl tetrazolium assay. To further investigate the effects of BA on septic cardiomyopathy, different concentrations of BA were used. The experiment was divided into control group, LPS induced- group, LPS+2.5, 5.0, 10.0 μM BA treatment group of the vitro model, and the Sham, CLP, CLP+10, 20, 30 mg/kg BA treatment groups of the rat vivo model. Lastly, cardiac injury, NLRP3 inflammation, and cardiac function were assessed in each group.
Results
The mRNA and protein expression of cardiac inflammation and injury genes were significantly increased in the in vitro and in vivo sepsis cardiomyopathy models. When different concentrations of BA were used in sepsis cardiomyopathy in vivo and in vitro, the above-mentioned myocardial inflammation and injury factors were suppressed to varying degrees, cell viability increased, cardiac function improved, and the survival rate of rats also increased.