Introduction:
Recently, enhanced activation of NLRP3 has been reported to be involved in atrial fibrillation (AF). This study aimed to detect the correlation between oxidative stress and NLRP3 and explore the role of miR-223-3p in the reactive oxygen species (ROS) injury induced by Ang II.

Material and methods:
Serum Ang II levels were examined using an ELISA kit. Fibrosis levels of right atrial appendages were determined by Masson’s staining. H9c2 cells transfected with miR-223-3p mimics were treated with Ang II with or without MCC950 (a potent selective NLRP3 inhibitor). Cell viability was detected by CCK-8 assay. Protein abundance was detected by Western blot. The malondialdehyde assay and DCFH-DA were used to measure oxidative stress. RT-qPCR was used to assay the expression of miR-223-3p and NLRP3.

Results:
In total, 43 patients enrolled in this study, including 20 patients with persistent (chronic) AF (cAF). Compared with the sinus rhythm (SR) group, we found enhanced activation of the NLRP3 inflammasome which was positively correlated with oxidative stress and serum Ang II level in cAF patients. Ang II induced ROS generation and inhibited H9c2 cell viability. In addition, overexpression of miR-223-3p functioned as MCC950 which inhibited expression of the NLRP3 inflammasome and partly attenuated the effects of ROS induced by Ang II on H9c2 cell viability. Lastly, we used luciferase assay to confirm NLRP3 as a direct target gene of miR-223-3p.

Conclusions:
miR-223-3p has protective effects on oxidative stress induced by Ang II in AF by targeting NLRP3 and could provide a new potential intervention target for treatment of AF.