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Propofol protects against high glucose-induced endothelial adhesion molecules expression in human umbilical vein endothelial cells

DOI: 10.1186/1475-2840-12-13

Keywords: Propofol, High glucose, Adhesion molecules, NF-κB, HUVECs

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Abstract:

Protein expression of endothelial adhesion molecules, NF-κB, inhibitory subunit of NF-κBα (IκBα), protein kinase Cβ2 (PKCβ2), and phosphorylation of PKCβ2 (Ser660) were measured by Western blot. NF-κB 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, PKCβ2 phosphorylation and PKC activation. Further, high glucose decreased IκBα expression in cytoplasm, increased the translocation of NF-κB from cytoplasm to nuclear, and induced NF-κB activation. Importantly, we found these high glucose-mediated effects were attenuated by propofol pretreatment. Moreover, CGP53353, a selective PKCβ2 inhibitor, decreased high glucose-induced NF-κB activation, adhesion molecules expression, and mononuclear-endothelial adhesion.Propofol, via decreasing O2.- accumulation, down-regulating PKCβ2 Ser660 phosphorylation and PKC as well as NF-κB 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

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