Furthermore, we illustrated that URB might inhibit CCH-induced activation of the NLRP3-CASP1 inflammasome pathway through the restoration of lysosomal function, and mitigate the impaired autophagy and mitophagy flux in part by preventing microglial overactivation and ROS accumulation, indicating that URB is a promising therapeutic agent for the treatment of CCH. This evidence concerns the gene NLRP3 and columnar cell hyperplasia of the breast.