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Captopril suppresses inflammation in endotoxin-induced uveitis in rats

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Title: Captopril suppresses inflammation in endotoxin-induced uveitis in rats
Authors: Ilieva, Iliyana Browse this author
Ohgami, Kazuhiro Browse this author →KAKEN DB
Jin, Xue-Hai Browse this author
Suzuki, Yukari Browse this author
Shiratori, Kenji Browse this author
Yoshida, Kazuhiko Browse this author →KAKEN DB
Kase, Satoru Browse this author →KAKEN DB
Ohno, Shigeaki Browse this author →KAKEN DB
Keywords: captopril
rennin-angiotensin system
anti-inflammatory agent
Issue Date: Sep-2006
Publisher: Elsevier B.V.
Journal Title: Experimental Eye Research
Volume: 83
Issue: 3
Start Page: 651
End Page: 657
Publisher DOI: 10.1016/j.exer.2006.03.005
PMID: 16698015
Abstract: Captopril is an inhibitor of angiotensin-converting enzyme (ACE) that is largely used in the treatment of cardiovascular diseases. Several previous studies have demonstrated that captopril exhibits a wide variety of biological activities, including an anti-inflammatory action, on which we focused our attention. The aim of the present study was to investigate the efficacy of captopril on endotoxin induced uveitis (EIU) in rats. We investigated its effect upon cellular infiltration and protein leakage, as well as on the concentration of tumor necrosis factor-α (TNF-α), nitric oxide (NO), prostaglandin E2 (PGE2), monocyte chemoattractant protein-1 (MCP-1) in the anterior chamber. In addition, we checked its effect on activation of nuclear factor kappa B (NF-κB) in iris and ciliary body (ICB) cells in vivo. EIU was induced in male Lewis rats by a footpad injection of lipopolysaccharide (LPS). One hour after the LPS inoculation, either 1 mg/kg, 10 mg/kg or 100 mg/kg captopril were injected intravenously. 24 h later, the aqueous humor was collected from both eyes, and the number of infiltrating cells and protein concentration in the aqueous humor were determined. Levels of TNF-α, PGE2, NO and MCP-1 were determined by enzyme-linked immunosorbent assay. On some eyes, after enucleation, immunohistochemical staining with a monoclonal antibody against activated NF-κB was performed. Captopril treatment significantly decreased the inflammatory cells infiltration, the level of protein, concentrations of TNF-α, PGE2, NO and MCP-1 in the aqueous humor. The number of activated NF-κB-positive cells was lower in ICB of the rats treated with captopril 3 h after the LPS injection. The present results indicate that captopril suppresses the inflammation in EIU by inhibiting the NF-κB-dependent pathway and the subsequent production of pro-inflammatory mediators.
Type: article (author version)
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)


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