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Author: Galimberti D. Baron P. Meda L. Prat E. Scarpini E. delgado R. Catania A. Lipton J.M. Scarlato G.
Publisher: Elsevier
ISSN: 0006-291X
Source: Biochemical and Biophysical Research Communications, Vol.263, Iss.1, 1999-09, pp. : 251-256
Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.
Abstract
α-Melanocyte stimulating hormone (α-MSH) is an ancient tridecapeptide with potent inhibitory activity in all major forms of inflammation. The anti-inflammatory message sequence of α-MSH resides in the COOH-terminal tripeptide α-MSH[11–13]. We tested the influence of α-MSH[1–13] and of α-MSH[11–13] in a cultured murine microglia cell line known to produce nitric oxide (NO-2) and tumor necrosis factor (TNFα) when stimulated with β-amyloid protein (Aβ). Melanocortin peptides significantly inhibited release of both NO-2 and TNFα into cell-free supernatants from microglia stimulated with Aβ[1–42] or Aβ[25–35] peptides and interferon γ (IFNγ). Northern blot analysis demonstrated that α-MSH[1–13] and α-MSH[11–13] inhibited accumulation of inducible nitric oxide synthase (iNOS) and TNFα mRNA was triggered by Aβ stimulation. Aβ/microglial interaction is believed to promote the progression of inflammatory and neurodegenerative changes in senile plaques in Alzheimer's disease. Our data indicate that α-MSH peptides might be used to modulate the local response of the brain to Aβ deposition in this neurodegenerative disease.
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