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.
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.