title: Anti-inflammatory activity of creatine supplementation in endothelial cells in vitro.
abstract: 1 Creatine (CR) supplementation augments muscle strength in skeletal muscle cells by increasing intracellular energy pools. However, the effect of CR supplementation on endothelial cells remains to be clarified. 2 In this study, we investigated whether CR supplementation had any anti-inflammatory activity against human pulmonary endothelial cells in culture. 3 We confirmed that supplementation with 0.5 mM CR significantly increased both intracellular CR and phosphocreatine (PC) through a CR transporter while keeping intracellular ATP levels constant independent of CR supplementation and a CR transporter antagonist. 4 In the assay system of endothelial permeability, supplementation with 5 mM CR significantly suppressed the endothelial permeability induced by serotonin and H(2)O(2). 5 In cell adhesion experiments, supplementation with 5 mM CR significantly suppressed neutrophil adhesion to endothelial cells. 6 In the measurement of adhesion molecules, CR supplementation with more than 0.5 mM CR significantly inhibited the expressions of ICAM-1 and E-selectin on endothelial cells, and the inhibition was significantly suppressed by an adenosine A(2A) receptor antagonist. 7 The present study suggests that CR supplementation has anti-inflammatory activities against endothelial cells.
authors.affiliation: Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tennoudai 1-1-1, Tsukuba, Ibaraki 305-8575, Japan.
authors.forename: Akihiro
authors.initials: A
authors.lastname: Nomura
authors.forename: Minjie
authors.initials: M
authors.lastname: Zhang
authors.forename: Tohru
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Yukio
authors.initials: Y
authors.lastname: Ishii
authors.forename: Yuko
authors.initials: Y
authors.lastname: Morishima
authors.forename: Mie
authors.initials: M
authors.lastname: Mochizuki
authors.forename: Toru
authors.initials: T
authors.lastname: Kimura
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Uchida
authors.forename: Kiyohisa
authors.initials: K
authors.lastname: Sekizawa
mesh_terms: D000255:Adenosine Triphosphate / Q000096:biosynthesis / Q000737:chemistry; D000893:Anti-Inflammatory Agents / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000493:pharmacokinetics; D002448:Cell Adhesion; D002478:Cells, Cultured; D003401:Creatine / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000493:pharmacokinetics*; D019587:Dietary Supplements; D019040:E-Selectin / Q000378:metabolism / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000737:chemistry / Q000166:cytology / Q000187:drug effects*; D006146:Guanidines / Q000494:pharmacology; D006801:Humans; D006861:Hydrogen Peroxide / Q000009:adverse effects; D007249:Inflammation / Q000139:chemically induced / Q000517:prevention & control*; D018799:Intercellular Adhesion Molecule-1; D007425:Intracellular Membranes / Q000187:drug effects; D008168:Lung / Q000098:blood supply; D018375:Neutrophil Activation / Q000187:drug effects; D009504:Neutrophils; D010539:Permeability / Q000187:drug effects; D010725:Phosphocreatine / Q000096:biosynthesis / Q000737:chemistry; D011422:Propionates / Q000494:pharmacology; D012701:Serotonin / Q000009:adverse effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism / Q000494:pharmacology
chemical_list: D000893:Anti-Inflammatory Agents; D019040:E-Selectin; D006146:Guanidines; D011422:Propionates; D014409:Tumor Necrosis Factor-alpha; D010725:Phosphocreatine; D018799:Intercellular Adhesion Molecule-1; D012701:Serotonin; D000255:Adenosine Triphosphate; D006861:Hydrogen Peroxide; D003401:Creatine; C005775:guanidinopropionic acid