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) (100?ng/mL) or with LPS plus vasopressin (10?pg/mL, 100?pg/mL, or 1000?pg/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-¦Á (TNF-¦Á), interleukin-1¦Â (IL-1¦Â), 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-¦Á (p?=?0.045 and p?=?0.007, respectively), IL-1¦Â (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.
