title: Anti-inflammatory effect of spironolactone on human peripheral blood mononuclear cells.
abstract: We evaluated the effect of alacepril, CV-11974, and spironolactone on the production of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) in cultured human peripheral blood mononuclear cells stimulated with angiotensin (Ang) II. Alacepril, CV-11974, and spironolactone significantly reduced the enhanced production of MCP-1 and TNF-alpha induced by exogenous Ang II. Specifically, 10 muM of spironolactone significantly reduced cytokine production, compared to the same dose of alacepril or CV-11974. These findings indicate that spironolactone may contribute to ameliorate the prognosis of patients with cardiovascular diseases by reducing Ang II-induced inflammation, although further exploration including determining the mechanisms would be required.
authors.affiliation: Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Japan. miura@mpc.t.u-tokyo.ac.jp
authors.forename: Ryuzea
authors.initials: R
authors.lastname: Miura
authors.forename: Kazufumi
authors.initials: K
authors.lastname: Nakamura
authors.forename: Daiji
authors.initials: D
authors.lastname: Miura
authors.forename: Aya
authors.initials: A
authors.lastname: Miura
authors.forename: Kenichi
authors.initials: K
authors.lastname: Hisamatsu
authors.forename: Masahito
authors.initials: M
authors.lastname: Kajiya
authors.forename: Satoshi
authors.initials: S
authors.lastname: Nagase
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Morita
authors.forename: Kengo
authors.initials: K
authors.lastname: Fukushima Kusano
authors.forename: Tohru
authors.initials: T
authors.lastname: Ohe
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Ishihara
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001562:Benzimidazoles / Q000494:pharmacology; D001713:Biphenyl Compounds; D002216:Captopril / Q000031:analogs & derivatives / Q000494:pharmacology; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology*; D013148:Spironolactone / Q000494:pharmacology*; D013777:Tetrazoles / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D000893:Anti-Inflammatory Agents; D001562:Benzimidazoles; D001713:Biphenyl Compounds; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D000451:Mineralocorticoid Receptor Antagonists; D013777:Tetrazoles; D014409:Tumor Necrosis Factor-alpha; D000804:Angiotensin II; D013148:Spironolactone; D002216:Captopril; C081643:candesartan; C046835:alacepril