Table 1 Agouti (endogenous MC1R inverse agonist) inhibits the effects of MECO-1 and alpha-MSH on endotoxin-stimulated TNF release

From: New melanocortin-like peptide of E. coli can suppress inflammation via the mammalian melanocortin-1 receptor (MC1R): possible endocrine-like function for microbes of the gut

Agouti (pM)

TNF-accumulated (% of control)

 

MECO-1 (10-12 M)

Alpha-MSH (10-12 M)

0

52.9 ± 11.2

67.05 ± 10.2

10

134.3 ± 14.5**

132.6 ± 4.9*

103

172.9 ± 10.1**

138.6 ± 12.4*

105

152.4 ± 6.1**

122.2 ± 4.3*

  1. The experiment was as described in the legend of Fig. 3 except that HMGB1 were replaced by LPS (10 ng/ml) and anti-receptor antibody was replaced by agouti, the endogenous peptide that is an inverse agonist of alpha-MSH action via MC1R. TNF release by LPS (10 ng/ml) alone was set at 100%
  2. **p<0.01 vs. MECO-1, *p<0.05 vs. alpha-MSH
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