NFKB1 and Hyperglycemia: Evidence suggests that the inhibitor exertsthis beneficial effect at least in part by regulating activation of thetranscription factor, NF-κB, and in particular, the p50 subunit of NF-κB. In bovine retinal endothelial cells, PARP interacts directly with subunits of NF-κB, and inhibition of PARP activity blocked the hyperglycemia-induced increase in NF-κB and proinflammatory geneproducts [72].