Diabetes-related complications in human and veterinary medicine have been shown to be associated with hyperglycemia-induced inflammation. It has been recently suggested that the onset of insulin resistance may be caused by over-production of inflammatory cytokines such as tumor necrosis factor (TNF)-${alpha}$ from immune cells. Conjugated linoleic acid (CLA) regulates inflammatory response through modulation of TNF-${alpha}$ expression. The objective of this study was to examine the effect of CLA on nuclear factor kappaB (NF-${kappa}B$) p65 binding activity, inhibitory kappaB ($I{kappa}B$)-${alpha}$ expression, and TNF-${alpha}$ production from high glucose-treated RAW 264.7 cells. CLA was added to RAW cells that had been previously cultured with low or high concentration of glucose. The levels of TNF-${alpha}$ protein in the culture supernatant of RAW cells exposed to high concentrations of glucose were higher than those of cells exposed to low concentrations of glucose. The treatment with the high concentration of glucose in RAW cells increased levels of NF-${kappa}B$ p65 binding activity and the decreased $I{kappa}B-{alpha}$ expression when compared with those of low glucose. The treatments in combination with CLA and glucose (low and high) glucose in RAW cells increased TNF-${alpha}$ production when compared with that glucose alone. These treatments with CLA increased TNF-${alpha}$ production in high glucose-treated RAW cells than those with low glucose. These treatments of CLA also showed higher NF-${kappa}B$ p65 binding activity and lower $I{kappa}B-{alpha}$ expression in high glucose than those in low glucose condition. This suggests that CLA can increase NF-${kappa}B$ p65 binding activity and TNF-${alpha}$ production from high glucose-treated RAW 264.7 cells and is likely to promote hyperglycemia-induced inflammation.