NFKB1 and Hyperglycemia: While the suppression of oxidative stress by agents targeting NF-κB (via PDTC), NADPH oxidase (via DPI or apocynin), and mitochondrial complex I (via rotenone) appeared to exacerbate the suppressive effects of hyperglycaemia on eEPC and OEC viability and proliferation rates (Chen et al. 2007), targeting of the same mechanisms attenuated such detrimental effects in mature endothelial cells, including HBMECs, and enhanced the overall unity and function of BBB (Ulker et al. 2004; Weidig et al. 2004; Allen and Bayraktutan 2009).