title: Cysteine, histidine and glycine exhibit anti-inflammatory effects in human coronary arterial endothelial cells.
abstract: The activation of nuclear factor-kappa B (NF-κB) in vascular endothelial cells may be involved in vascular pathogeneses such as vasculitis or atherosclerosis. Recently, it has been reported that some amino acids exhibit anti-inflammatory effects. We investigated the inhibitory effects of a panel of amino acids on cytokine production or expression of adhesion molecules that are involved in inflammatory diseases in various cell types. The activation of NF-κB was determined in human coronary arterial endothelial cells (HCAECs) because NF-κB modulates the production of many cytokines and the expression of adhesion molecules. We examined the inhibitory effects of the amino acids cysteine, histidine and glycine on the induction of NF-κB activation, expression of CD62E (E-selectin) and the production of interleukin (IL)-6 in HCAECs stimulated with tumour necrosis factor (TNF)-α. Cysteine, histidine and glycine significantly reduced NF-κB activation and inhibitor κBα (IκBα) degradation in HCAECs stimulated with TNF-α. Additionally, all the amino acids inhibited the expression of E-selectin and the production of IL-6 in HCAECs, and the effects of cysteine were the most significant. Our results show that glycine, histidine and cysteine can inhibit NF-κB activation, IκBα degradation, CD62E expression and IL-6 production in HCAECs, suggesting that these amino acids may exhibit anti-inflammatory effects during endothelial inflammation.
authors.affiliation: Department of Pediatrics, Yamaguchi University Graduate School of Medicine, Ube, Japan. shunji@yamaguchi-u.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Hasegawa
authors.forename: T
authors.initials: T
authors.lastname: Ichiyama
authors.forename: I
authors.initials: I
authors.lastname: Sonaka
authors.forename: A
authors.initials: A
authors.lastname: Ohsaki
authors.forename: S
authors.initials: S
authors.lastname: Okada
authors.forename: H
authors.initials: H
authors.lastname: Wakiguchi
authors.forename: K
authors.initials: K
authors.lastname: Kudo
authors.forename: S
authors.initials: S
authors.lastname: Kittaka
authors.forename: M
authors.initials: M
authors.lastname: Hara
authors.forename: S
authors.initials: S
authors.lastname: Furukawa
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001167:Arteritis / Q000517:prevention & control*; D002478:Cells, Cultured / Q000187:drug effects / Q000378:metabolism; D003331:Coronary Vessels / Q000166:cytology*; D003545:Cysteine / Q000494:pharmacology*; D004353:Drug Evaluation, Preclinical; D019040:E-Selectin / Q000096:biosynthesis / Q000235:genetics; D042783:Endothelial Cells / Q000187:drug effects* / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology; D005786:Gene Expression Regulation / Q000187:drug effects; D005998:Glycine / Q000494:pharmacology*; D006639:Histidine / Q000494:pharmacology*; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D000893:Anti-Inflammatory Agents; D019040:E-Selectin; D020672:I-kappa B Proteins; C508600:IL6 protein, human; D015850:Interleukin-6; D016328:NF-kappa B; C000606204:NFKBIA protein, human; D014409:Tumor Necrosis Factor-alpha; D000072000:NF-KappaB Inhibitor alpha; D006639:Histidine; D003545:Cysteine; D005998:Glycine