Journal Browser Advanced Search Help
Journal Browser Advanced search HELP
Korean J Crit Care Med. 2015 Aug;30(3):151-157. English. In Vitro. https://doi.org/10.4266/kjccm.2015.30.3.151
Park J , Eo EY , Lee KH , Park JS , Lee JH , Yoo CG , Lee CT , Cho YJ .
Division of Pulmonology, Department of Internal Medicine, Bundang CHA Hospital, Seongnam, Korea.
Department of Internal Medicine, Respiratory Center, Seoul National University Bundang Hospital, Seongnam, Korea. lungdrcho@gmail.com
Division of Pulmonology and Critical Care Medicine, Department of Internal Medicine, Lung Institute, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
Abstract

BACKGROUND: Arginine vasopressin (AVP) is widely used as a vasopressor agent. Some recent studies have suggested that AVP may exert an immunomodulatory effect. However, the mechanism about the anti-inflammatory effect of AVP is not well known. We investigated the effect of AVP on the ihibitor of kappa B (IkappaBalpha)/nuclear factor-kappa B (NF-kappaB) pathway in RAW 264.7 cells. METHODS: Cultured RAW 264.7 cells were pretreated with AVP and stimulated with lipopolysaccharide (LPS). To evaluate the effect of AVP on inflammatory cytokines, the concentration of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were assessed by an enzyme-linked immunosorbent assay technique. The expression of IkappaBalpha and nuclear translocation of NF-kappaB p65 were measured by Western blotting, and IkappaB kinase (IKK) activity was analyzed by an in vitro immune complex kinase assay. To confirm the AVP effect on IkappaBalpha/NF-kappaB cascade and via V2 receptor, we added tolvaptan (V2 receptor antagonist) after AVP pretreatment. RESULTS: The increase of IL-6 and TNF-alpha in LPS-stimulated RAW 264.7 cells was suppressed by a treatment with AVP. Pretreatment of AVP inhibited increasing of IKK activity and IkappaBalpha degradation induced by LPS in RAW 264.7 cells. Furthermore, LPS induced and NF-kappaB transcription was inhibited by AVP pretreatment. The observed changes in IKK activity, IkappaBalpha degradation and NF-kappaB transcription by AVP was abolished by tolvaptan treatment. CONCLUSIONS: Our results suggest that AVP showed anti-inflammatory effect on LPS-induced IkappaBalpha/NF-kappaB cascade in mouse macrophages via V2 receptors.

Copyright © 2019. Korean Association of Medical Journal Editors.