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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 PPARs transcription and expression. PPAR-α and PPAR-γ transcription and expression were evaluated in primary astrocytes after 24 hrs of exposure to Aβ (1 μg/ml), in the presence or absence of PEA (10−7 M). (A) Results of PPAR-α and PPAR-γ Western blot analysis and densitometric analysis of corresponding bands. β-actin was used as loading control. (B) Results of PPAR-α and PPAR-γ RT-PCR amplification and densitometric analysis of corresponding bands. GAPDH was used as standard control. Each bar shows the mean ± S.E.M. of n = 4 separate experiments. ***P < 0.001 and *P < 0.05 versus control; ##P < 0.01 and #P < 0.05 versus Aβ-challenged cells.
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fig06: PEA effect on PPARs transcription and expression. PPAR-α and PPAR-γ transcription and expression were evaluated in primary astrocytes after 24 hrs of exposure to Aβ (1 μg/ml), in the presence or absence of PEA (10−7 M). (A) Results of PPAR-α and PPAR-γ Western blot analysis and densitometric analysis of corresponding bands. β-actin was used as loading control. (B) Results of PPAR-α and PPAR-γ RT-PCR amplification and densitometric analysis of corresponding bands. GAPDH was used as standard control. Each bar shows the mean ± S.E.M. of n = 4 separate experiments. ***P < 0.001 and *P < 0.05 versus control; ##P < 0.01 and #P < 0.05 versus Aβ-challenged cells.

Mentions: Additional experiments were aimed at investigating whether exposure to Aβ was able to affect PPAR transcription and expression. RT-PCR and Western blot analyses revealed that Aβ significantly down-regulated PPAR-α, but not PPAR-γ, transcription and expression. In the same experimental conditions, PEA was able to counteract the above reported alterations induced by Aβ (Fig. 6).


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 PPARs transcription and expression. PPAR-α and PPAR-γ transcription and expression were evaluated in primary astrocytes after 24 hrs of exposure to Aβ (1 μg/ml), in the presence or absence of PEA (10−7 M). (A) Results of PPAR-α and PPAR-γ Western blot analysis and densitometric analysis of corresponding bands. β-actin was used as loading control. (B) Results of PPAR-α and PPAR-γ RT-PCR amplification and densitometric analysis of corresponding bands. GAPDH was used as standard control. Each bar shows the mean ± S.E.M. of n = 4 separate experiments. ***P < 0.001 and *P < 0.05 versus control; ##P < 0.01 and #P < 0.05 versus Aβ-challenged cells.
© Copyright Policy
Related In: Results  -  Collection

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

fig06: PEA effect on PPARs transcription and expression. PPAR-α and PPAR-γ transcription and expression were evaluated in primary astrocytes after 24 hrs of exposure to Aβ (1 μg/ml), in the presence or absence of PEA (10−7 M). (A) Results of PPAR-α and PPAR-γ Western blot analysis and densitometric analysis of corresponding bands. β-actin was used as loading control. (B) Results of PPAR-α and PPAR-γ RT-PCR amplification and densitometric analysis of corresponding bands. GAPDH was used as standard control. Each bar shows the mean ± S.E.M. of n = 4 separate experiments. ***P < 0.001 and *P < 0.05 versus control; ##P < 0.01 and #P < 0.05 versus Aβ-challenged cells.
Mentions: Additional experiments were aimed at investigating whether exposure to Aβ was able to affect PPAR transcription and expression. RT-PCR and Western blot analyses revealed that Aβ significantly down-regulated PPAR-α, but not PPAR-γ, transcription and expression. In the same experimental conditions, PEA was able to counteract the above reported alterations induced by Aβ (Fig. 6).

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