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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.

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Related in: MedlinePlus

PEA effect on cannabinoid receptors expression. The expression of CB1 and CB2 receptors was evaluated in primary astrocytes after 24 hrs of exposure to Aβ (1 μg/ml), in the presence or absence of PEA (10−7 M). Figure shows the results of Western blot and densitometric analysis of corresponding bands. β-actin was used as loading control. Each bar shows the mean ± S.E.M. of n = 4 independent experiments. **P < 0.01 and *P < 0.05 versus control.
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fig07: PEA effect on cannabinoid receptors expression. The expression of CB1 and CB2 receptors was evaluated in primary astrocytes after 24 hrs of exposure to Aβ (1 μg/ml), in the presence or absence of PEA (10−7 M). Figure shows the results of Western blot and densitometric analysis of corresponding bands. β-actin was used as loading control. Each bar shows the mean ± S.E.M. of n = 4 independent experiments. **P < 0.01 and *P < 0.05 versus control.

Mentions: When astrocytes were treated under the same conditions which lead to inflammation, an important increase in CB2 expression and a significant decrease in CB1 expression were observed (Fig. 7). In addition, Aβ exposure induced a marked increase in astrocyte levels of the endocannabinoid 2-AG, the preferential agonist at CB2 receptor. Moreover, the peptide challenge resulted in a clear enhancement of PEA and OEA, both able to bind to PPPAR-α. Treatment of astrocytes with PEA (10−7 M) alone resulted in an elevation of 2-AG levels. The effects of Aβ and PEA were not additive. In no other case were levels of the other endocannabinoid, AEA, significantly altered (Table 1).


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 effect on cannabinoid receptors expression. The expression of CB1 and CB2 receptors was evaluated in primary astrocytes after 24 hrs of exposure to Aβ (1 μg/ml), in the presence or absence of PEA (10−7 M). Figure shows the results of Western blot and densitometric analysis of corresponding bands. β-actin was used as loading control. Each bar shows the mean ± S.E.M. of n = 4 independent experiments. **P < 0.01 and *P < 0.05 versus control.
© Copyright Policy
Related In: Results  -  Collection

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

fig07: PEA effect on cannabinoid receptors expression. The expression of CB1 and CB2 receptors was evaluated in primary astrocytes after 24 hrs of exposure to Aβ (1 μg/ml), in the presence or absence of PEA (10−7 M). Figure shows the results of Western blot and densitometric analysis of corresponding bands. β-actin was used as loading control. Each bar shows the mean ± S.E.M. of n = 4 independent experiments. **P < 0.01 and *P < 0.05 versus control.
Mentions: When astrocytes were treated under the same conditions which lead to inflammation, an important increase in CB2 expression and a significant decrease in CB1 expression were observed (Fig. 7). In addition, Aβ exposure induced a marked increase in astrocyte levels of the endocannabinoid 2-AG, the preferential agonist at CB2 receptor. Moreover, the peptide challenge resulted in a clear enhancement of PEA and OEA, both able to bind to PPPAR-α. Treatment of astrocytes with PEA (10−7 M) alone resulted in an elevation of 2-AG levels. The effects of Aβ and PEA were not additive. In no other case were levels of the other endocannabinoid, AEA, significantly altered (Table 1).

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