Limits...
Palmitoylethanolamide counteracts reactive astrogliosis induced by β-amyloid peptide.

Scuderi C, Esposito G, Blasio A, Valenza M, Arietti P, Steardo L, Carnuccio R, De Filippis D, Petrosino S, Iuvone T, Di Marzo V, Steardo L - J. Cell. Mol. Med. (2011)

Bottom Line: This effect was reduced by PPAR-α antagonist.Moreover, this ALIAmide, like Aβ, increased 2-AG levels.These results indicate that PEA exhibits anti-inflammatory properties able to counteract Aβ-induced astrogliosis, and suggest novel treatment for neuroinflammatory/ neurodegenerative processes.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Sapienza University of Rome, Rome, Italy.

Show MeSH

Related in: MedlinePlus

PEA effects on Aβ-induced pro-inflammatory cytokine release. Aβ-challenged (1 μg/ml) cells were treated with PEA (10−7 M) in the presence of the selective PPAR-γ antagonist (GW9662, 9 nM) or the selective PPAR-α antagonist (MK886, 3 μM). TNF-α and IL-1β release was measured after 24 hrs of treatments by ELISA assay. Each bar shows the mean ± S.E.M. of n = 3 separate experiments. ***P < 0.001 versus control; ###P < 0.001 versus Aβ-challenged cells; °P < 0.05 versus Aβ+ PEA-challenged cells.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4373435&req=5

fig03: PEA effects on Aβ-induced pro-inflammatory cytokine release. Aβ-challenged (1 μg/ml) cells were treated with PEA (10−7 M) in the presence of the selective PPAR-γ antagonist (GW9662, 9 nM) or the selective PPAR-α antagonist (MK886, 3 μM). TNF-α and IL-1β release was measured after 24 hrs of treatments by ELISA assay. Each bar shows the mean ± S.E.M. of n = 3 separate experiments. ***P < 0.001 versus control; ###P < 0.001 versus Aβ-challenged cells; °P < 0.05 versus Aβ+ PEA-challenged cells.

Mentions: Another set of experiments was aimed at assessing the effect of PEA on the production of inflammatory factors induced by Aβ. Treatment with Aβ for 24 hrs resulted in a significant increase in iNOS and COX-2 expression, as determined by Western blot and immunofluorescence analyses. Such protein increase paralleled nitric oxide, IL-1β, TNF-α and PGE2 up-release, as determined by Griess reaction and ELISA experiments. Also in this case PEA antagonized the enhancement of both expression and release of all pro-inflammatory molecules detected, and the blockade of PPAR-α with MK886 partly attenuated these effects (Figs 2 and 3).


Palmitoylethanolamide counteracts reactive astrogliosis induced by β-amyloid peptide.

Scuderi C, Esposito G, Blasio A, Valenza M, Arietti P, Steardo L, Carnuccio R, De Filippis D, Petrosino S, Iuvone T, Di Marzo V, Steardo L - J. Cell. Mol. Med. (2011)

PEA effects on Aβ-induced pro-inflammatory cytokine release. Aβ-challenged (1 μg/ml) cells were treated with PEA (10−7 M) in the presence of the selective PPAR-γ antagonist (GW9662, 9 nM) or the selective PPAR-α antagonist (MK886, 3 μM). TNF-α and IL-1β release was measured after 24 hrs of treatments by ELISA assay. Each bar shows the mean ± S.E.M. of n = 3 separate experiments. ***P < 0.001 versus control; ###P < 0.001 versus Aβ-challenged cells; °P < 0.05 versus Aβ+ PEA-challenged cells.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4373435&req=5

fig03: PEA effects on Aβ-induced pro-inflammatory cytokine release. Aβ-challenged (1 μg/ml) cells were treated with PEA (10−7 M) in the presence of the selective PPAR-γ antagonist (GW9662, 9 nM) or the selective PPAR-α antagonist (MK886, 3 μM). TNF-α and IL-1β release was measured after 24 hrs of treatments by ELISA assay. Each bar shows the mean ± S.E.M. of n = 3 separate experiments. ***P < 0.001 versus control; ###P < 0.001 versus Aβ-challenged cells; °P < 0.05 versus Aβ+ PEA-challenged cells.
Mentions: Another set of experiments was aimed at assessing the effect of PEA on the production of inflammatory factors induced by Aβ. Treatment with Aβ for 24 hrs resulted in a significant increase in iNOS and COX-2 expression, as determined by Western blot and immunofluorescence analyses. Such protein increase paralleled nitric oxide, IL-1β, TNF-α and PGE2 up-release, as determined by Griess reaction and ELISA experiments. Also in this case PEA antagonized the enhancement of both expression and release of all pro-inflammatory molecules detected, and the blockade of PPAR-α with MK886 partly attenuated these effects (Figs 2 and 3).

Bottom Line: This effect was reduced by PPAR-α antagonist.Moreover, this ALIAmide, like Aβ, increased 2-AG levels.These results indicate that PEA exhibits anti-inflammatory properties able to counteract Aβ-induced astrogliosis, and suggest novel treatment for neuroinflammatory/ neurodegenerative processes.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Sapienza University of Rome, Rome, Italy.

Show MeSH
Related in: MedlinePlus