MicroRNA-223 regulates inflammation and brain injury via feedback to NLRP3 inflammasome after intracerebral hemorrhage

• miR-223 could downregulate NLRP3 to inhibit inflammation through caspase-1 and IL-1β.
• miR-223 could reduce brain edema and improve neurological functions.
• miR-223 represents a novel target reducing the inflammatory response.

NLRP3 inflammasome, the multimeric protein complexes involved in the processing of IL-1β through Caspase-1 cleavage, facilitates the inflammatory response. The control and activation of NLRP3 after intracerebral hemorrhage have not been fully studied. In the current study, we explore the specific microRNA which could regulate the NLRP3 inflammasome and inflammation after intracerebral hemorrhage. We detected the inverse relationship between the expression of miR-223 and NLRP3. We found that NLRP3 mRNA contains conserved miR-223 binding sites in its 3′ UTR, and miR-223 could directly regulate NLRP3 expression through these 3′ UTR sites. Our results indicate that miR-223 could downregulate NLRP3 to inhibit inflammation through caspase-1 and IL-1β, reduce brain edema and improve neurological functions. Together, miR-223 may be a vital regulator of NLRP3 inflammasome activation. The results suggest that miR-223 represents a novel target reducing the inflammatory response, and offers a new therapeutical strategy following ICH.