These data indicate that high glucose concentration and hyperglycemia promote leukocyte adhesion to the endothelium through upregulation of cell surface expression of adhesive proteins, possibly depending on NF-kB activation.
The apparent mechanism of NAT for its nephroprotection may be due to the suppression of hyperglycemia-mediated oxidative stress and amelioration of inflammatory cascades allied with NF-kB activation.
I/R-induced increases in HMGB1 and Toll-like receptors (TLRs), activation of NF-kB, and resultant alterations in interleukin-1β, tumor necrosis factor-α, proapoptotic Bax, and antiapoptotic Bcl-2 were all favorably modulated by EP treatment in both the NG and HG groups compared with their corresponding control groups.
Meanwhile, PNS remarkably increased the protein expression of arginase 1 and decreased I<i>κ</i>B-alpha phosphorylation and subunits of NF-<i>κ</i>B p50 and p65 from macrophages in culture medium with hyperglycemia.