Conclusion
This study highlights that up-regulated miR-221-3p suppresses the overactivation of NLRP3/ASC/pro-caspase-1 inflammasome pathway and has an anti-inflammatory effect in CHD. Thus, miR-221-3p may serve as a potential target for the treatment of CHD.
Methods
Sixty CHD patients and 60 healthy controls were collected to detect the expression of miR-221-3p, NLRP3, ASC, pro-caspase-1 in peripheral blood and the contents of related factors in serum. The rats model of CHD was injected with miR-221-3p agomir or miR-221-3p antagomir to explore its functions in miR-221-3p, NLRP3, ASC and pro-caspase-1 expression, electrocardiogram data, cardiomyocytes apoptosis, myocardial injury, inflammatory reaction and oxidative stress of CHD rats.
Objective
As some evidence has demonstrated the role of microRNA-221 (miR-221) on coronary heart disease (CHD), the aim of the present study was to investigate the effect of miR-221-3p on CHD via regulating NLRP3/ASC/pro-caspase-1 inflammasome pathway.
Results
MiR-221-3p declined and NLRP3, ASC and pro-caspase-1 raised in CHD. Up-regulated miR-221-3p reduced the change value of J-point and T-wave, decreased NLRP3, ASC and pro-caspase-1 expression, suppressed apoptosis in cardiomyocytes, as well as suppressed myocardial injury, inflammatory reaction and oxidative stress in CHD rats.