Objectives: We sought to elucidate the effects of vasopressin on modulating the endotoxin-induced upregulation of inflammatory mediators. Materials and Methods: A confluent murine macrophage-like cell line, RAW264.7 cells, were treated with lipopolysaccharide (LPS) (100ng/mL) or with LPS plus vasopressin (10pg/mL, 100pg/mL, or 1000pg/mL); the cells were denoted as the LPS group, the LPS-V(10) group, the LPS-V(100) group, and the LPS-V(1000) group, respectively. The respective control groups were run simultaneously. Vasopressin was administered immediately after LPS. The expression of inflammatory molecules was then assayed. The molecules that were assayed included the chemokine macrophage-inflammatory protein-2 (MIP-2); the cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6); nitric oxide (NO)/inducible NO synthase (iNOS); and prostaglandin E2 (PGE2)/cyclooxygenase-2 (COX-2). Results: The differences between the LPS and LPS-V(10) groups in the concentration of inflammatory mediators were not statistically significant. By contrast, the LPS-V(100) and LPS-V(1000) groups were significantly lower than the LPS group in the concentration of MIP-2 (p=0.004 and p=0.001, respectively), TNF-α (p=0.045 and p=0.007, respectively), IL-1β (p=0.003 and p<0.001, respectively), NO (p=0.014 and p=0.001, respectively), iNOS mRNA (p=0.001 and p<0.001, respectively), PGE2 (p=0.021 and p<0.001, respectively), and COX-2 mRNA (p=0.021 and p=0.006, respectively). The IL-6 concentration was moreover significantly lower in the LPS-V(1000) group than in the LPS group (p<0.001), whereas the IL-6 concentration in the LPS-V(100) and the LPS groups was not significantly different. Conclusion: In a dose-dependent manner, vasopressin inhibited the endotoxin-induced upregulation of inflammatory mediators in activated murine macrophages.
ASJC Scopus subject areas
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