%0 Journal Article %T Propofol protects against high glucose-induced endothelial adhesion molecules expression in human umbilical vein endothelial cells %A Minmin Zhu %A Jiawei Chen %A Hui Jiang %A Changhong Miao %J Cardiovascular Diabetology %D 2013 %I BioMed Central %R 10.1186/1475-2840-12-13 %X Protein expression of endothelial adhesion molecules, NF-百B, inhibitory subunit of NF-百B汐 (I百B汐), protein kinase C汕2 (PKC汕2), and phosphorylation of PKC汕2 (Ser660) were measured by Western blot. NF-百B activity was measured by electrophoretic mobility shift assay. PKC activity was measured with SignaTECT PKC assay system. Superoxide anion (O2.-) accumulation was measured with the reduction of ferricytochrome c assay. Human peripheral mononuclear cells were prepared with Histopaque-1077 solution.High glucose induced the expression of endothelial selectin (E-selectin), intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and increased mononuclear-endothelial adhesion. High glucose induced O2.- accumulation, PKC汕2 phosphorylation and PKC activation. Further, high glucose decreased I百B汐 expression in cytoplasm, increased the translocation of NF-百B from cytoplasm to nuclear, and induced NF-百B activation. Importantly, we found these high glucose-mediated effects were attenuated by propofol pretreatment. Moreover, CGP53353, a selective PKC汕2 inhibitor, decreased high glucose-induced NF-百B activation, adhesion molecules expression, and mononuclear-endothelial adhesion.Propofol, via decreasing O2.- accumulation, down-regulating PKC汕2 Ser660 phosphorylation and PKC as well as NF-百B activity, attenuated high glucose-induced endothelial adhesion molecules expression and mononuclear-endothelial adhesion.Perioperative hyperglycemia, a metabolic alteration caused by perioperative physiological stress and excessive glucose infusion, was commonly seen in non-diabetics [1] as well as diabetics [2]. Hyperglycemia could up-regulate the expression of endothelial adhesion molecules, such as endothelial selectin (E-selectin), intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) [3-5], thus augmenting pathological leukocytes-endothelial adhesion [3] and leading to endothelial dysfunction and injury. Accordingly, during %K Propofol %K High glucose %K Adhesion molecules %K NF-百B %K HUVECs %U http://www.cardiab.com/content/12/1/13