The Anti-Inflammatory Effect of Arginine-Vasopressin on Lipopolysaccharide-Induced IkappaBalpha/Nuclear Factor-kappaB Cascade.
10.4266/kjccm.2015.30.3.151
- Author:
Jisoo PARK
;
Eun Young EO
;
Kyoung Hee LEE
;
Jong Sun PARK
;
Jae Ho LEE
;
Chul Gyu YOO
;
Choon Taek LEE
;
Young Jae CHO
- Publication Type:In Vitro ; Original Article
- Keywords:
anti-inflammatory effect;
arginine Vasopressin;
IkappaBalpha;
NF-kappaB
- MeSH:
Animals;
Antigen-Antibody Complex;
Arginine Vasopressin;
Blotting, Western;
Cytokines;
Enzyme-Linked Immunosorbent Assay;
I-kappa B Kinase;
Interleukin-6;
Macrophages;
Mice;
NF-kappa B;
Phosphotransferases;
Receptors, Vasopressin;
Tumor Necrosis Factor-alpha
- From:Korean Journal of Critical Care Medicine
2015;30(3):151-157
- CountryRepublic of Korea
- Language:English
-
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.
