title: Lycopus lucidus inhibits high glucose-induced vascular inflammation in human umbilical vein endothelial cells.
abstract: Vascular inflammatory process has been suggested to play a key role in the initiation and progression of atherosclerosis, a major complication of diabetes mellitus. Lycopus lucidus Turcz. has been used as an oriental traditional medicine including Korea and its crude drug is known to have an anti-inflammatory effect. Thus we investigated whether the aqueous extract of the leaves of L. lucidus Turcz. (ALT) suppresses vascular inflammatory process induced by high glucose in primary cultured human umbilical vein endothelial cells (HUVEC). Western blot analysis revealed that incubation of HUVEC with high glucose increased cell adhesion molecules (CAMs) expression levels. However, high glucose-induced increase of CAMs expression was significantly attenuated by pretreatment with ALT in a dose-dependent manner. The enhanced cell adhesion between monocyte and HUVEC induced by high glucose was also blocked by pretreatment with ALT. High glucose-induced hydrogen peroxide production and DCF-sensitive intracellular reactive oxygen species (ROS) formation. Pretreatment with ALT inhibited high glucose-induced ROS formation. In addition, ALT suppressed the translocation and promoter transcriptional activity of NF-kappaB increased in high glucose condition. Taken together, the present data suggested that ALT could suppress high glucose-induced vascular inflammatory process, which may be closely related with the inhibition of ROS and NF-kappaB activation in HUVEC.
authors: Professional Graduate School of Oriental Medicine, Republic of Korea.
authors: Yun Jung
authors: YJ
authors: Lee
authors: Dae Gill
authors: DG
authors: Kang
authors: Jin Sook
authors: JS
authors: Kim
authors: Ho Sub
authors: HS
authors: Lee
mesh_terms: D000893:Anti-Inflammatory Agents / Q000302:isolation & purification / Q000494:pharmacology*; D015153:Blotting, Western; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D019040:E-Selectin / Q000235:genetics / Q000378:metabolism; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005947:Glucose / Q000494:pharmacology*; D018922:HL-60 Cells; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D008156:Luciferases / Q000235:genetics / Q000378:metabolism; D031333:Lycopus / Q000737:chemistry*; D008856:Microscopy, Fluorescence; D016328:NF-kappa B / Q000378:metabolism; D010936:Plant Extracts / Q000302:isolation & purification / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014162:Transfection; D014471:Umbilical Veins / Q000166:cytology; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D019040:E-Selectin; D016209:Interleukin-8; D016328:NF-kappa B; D010936:Plant Extracts; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D006861:Hydrogen Peroxide; D008156:Luciferases; D005947:Glucose