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.
Under hyperglycemia, cAMP production and PKA activity were markedly increased as a result of glucose transporter 1-mediated glucose influx that drives glucose metabolism and ATP production, which led to increased phosphorylation of p65 and CREB.
HMVRECs were treated with hyperglycemia (HG) or euglycemia and mRNA and protein levels of TLR-2, TLR-4, MyD88, IRF3, and TRIF as well as NF-κB p65 activation were measured.
Experimental evidence indicates that previous hyperglycemia is associated with persistent expression of the NFκB p65 gene, which activates NFκB-dependent proteins, such as MCP-1, which are implicated in diabetes-associated vascular injury.
Hyperglycemia-induced epigenetic changes and increased p65 expression are prevented by reducing mitochondrial superoxide production or superoxide-induced alpha-oxoaldehydes.