Nice find Topcoin. I found what you were referring to in these two posters:

https://www.resverlogix.com/upload/media_element/170/b7205a7c7187/eas-2019-poster-nw-final-final.pdf

https://www.resverlogix.com/upload/media_element/168/2d3efd79784a/vascular-discovery-2019-vi-bioinformatics-poster.pdf

Seems that in the human umbilical vein endothelial cells (HUVECs), that 24 hour treatement with high-glucose condition (25 mM for 24 hours) induces a 1.7-fold increase in the mRNA level of NLRP3. Co-treatement with 5 uM or 20 uM apabetalone attenuated this high-glucose effect by 20% and 44%, respectively. 

One thing to keep in mind is that the NLRP3 inflammasome pathway is extremely complex and involves both priming and activation steps. One function of the priming step is to transcriptionally upregulate the mRNAs encoding inflammasome components, including but not limited to NLRP3. This is likely where apabetalone fits in with the HUVEC NLRP3 mRNA observation.

Priming also involves post-translational changes to the NLRP3 protein that stabilize and ready it for subsequent activation by pro-inflammatory stimuli. The full activation of the NLRP3 inflammasome is quite complex and elicits several downstream effects. Those reviews I linked to earlier go into more detail if anyone cares look further. Apabetalone may play a role here in NLRP3 activation as well, but cannot be concluded just from NLRP3 mRNA data in those posters.

BearDownAZ