Vasopressin inhibits endotoxin-induced upregulation of inflammatory mediators in activated macrophages

Tsui Chin Peng, Chun Jen Huang

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)150-154
Number of pages5
JournalTzu Chi Medical Journal
Volume25
Issue number3
DOIs
Publication statusPublished - Sep 2013
Externally publishedYes

Fingerprint

Vasopressins
Endotoxins
Lipopolysaccharides
Up-Regulation
Macrophages
Chemokine CXCL2
Interleukin-6
Cyclooxygenase 2
Interleukin-1
Dinoprostone
Nitric Oxide
Tumor Necrosis Factor-alpha
Messenger RNA
Nitric Oxide Synthase Type II
Prostaglandin-Endoperoxide Synthases
Chemokines
Nitric Oxide Synthase

Keywords

  • Chemokine
  • Cytokine
  • Lipopolysaccharide
  • Nitric oxide
  • Prostaglandin E

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Vasopressin inhibits endotoxin-induced upregulation of inflammatory mediators in activated macrophages. / Peng, Tsui Chin; Huang, Chun Jen.

In: Tzu Chi Medical Journal, Vol. 25, No. 3, 09.2013, p. 150-154.

Research output: Contribution to journalArticle

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abstract = "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.",
keywords = "Chemokine, Cytokine, Lipopolysaccharide, Nitric oxide, Prostaglandin E",
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T1 - Vasopressin inhibits endotoxin-induced upregulation of inflammatory mediators in activated macrophages

AU - Peng, Tsui Chin

AU - Huang, Chun Jen

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N2 - 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.

AB - 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.

KW - Chemokine

KW - Cytokine

KW - Lipopolysaccharide

KW - Nitric oxide

KW - Prostaglandin E

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