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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 attenuates Aβ-induced astrocyte activation. 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). GFAP mRNA was evaluated 12 hrs following Aβ challenge; GFAP and S100B protein expression was evaluated after 24 hrs of treatments by Western blot and immunofluorescence analyses. S100B release in the cellular milieu was determined 24 hrs after Aβ challenge by ELISA assay. (A) Results of GFAP and S100B Western blot analysis and densitometric analysis of corresponding bands. β-actin was used as loading control. (B) Results of GFAP RT-PCR amplification and densitometric analysis of corresponding bands. GAPDH was used as standard control. (C) Measurement of S100B release by ELISA assay. (D) Analysis of GFAP and S100B protein expression by immunofluorescence (magnification 10 × ). Results are the mean ± S.E.M. of n = 4 separate experiments. ***P < 0.001 versus control; ###P < 0.01 versus Aβ-challenged cells; °°°P < 0.001 and °P < 0.05 versus Aβ+ PEA-challenged cells.
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fig01: PEA attenuates Aβ-induced astrocyte activation. 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). GFAP mRNA was evaluated 12 hrs following Aβ challenge; GFAP and S100B protein expression was evaluated after 24 hrs of treatments by Western blot and immunofluorescence analyses. S100B release in the cellular milieu was determined 24 hrs after Aβ challenge by ELISA assay. (A) Results of GFAP and S100B Western blot analysis and densitometric analysis of corresponding bands. β-actin was used as loading control. (B) Results of GFAP RT-PCR amplification and densitometric analysis of corresponding bands. GAPDH was used as standard control. (C) Measurement of S100B release by ELISA assay. (D) Analysis of GFAP and S100B protein expression by immunofluorescence (magnification 10 × ). Results are the mean ± S.E.M. of n = 4 separate experiments. ***P < 0.001 versus control; ###P < 0.01 versus Aβ-challenged cells; °°°P < 0.001 and °P < 0.05 versus Aβ+ PEA-challenged cells.

Mentions: In order to test the effect of PEA on Aβ-induced astrogliosis, the expression of GFAP and S100B, specific markers of astrocyte activity, was explored. Reactive astrocytes display hypertrophied cell bodies and thickened processes exhibiting GFAP-immunoreactivity. Using immunofluorescence, Western blot and RT-PCR analyses, we observed a marked increase in both transcription and expression of GFAP after Aβ challenge. This enhancement was significantly attenuated by PEA treatment. Moreover, the PPAR-α antagonist MK886 was able to partly blunt the PEA-induced attenuation of GFAP transcription and expression. Such effect indicated a significant, although not exclusive, involvement of the PPAR-α receptor in mediating PEA action (Fig. 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 attenuates Aβ-induced astrocyte activation. 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). GFAP mRNA was evaluated 12 hrs following Aβ challenge; GFAP and S100B protein expression was evaluated after 24 hrs of treatments by Western blot and immunofluorescence analyses. S100B release in the cellular milieu was determined 24 hrs after Aβ challenge by ELISA assay. (A) Results of GFAP and S100B Western blot analysis and densitometric analysis of corresponding bands. β-actin was used as loading control. (B) Results of GFAP RT-PCR amplification and densitometric analysis of corresponding bands. GAPDH was used as standard control. (C) Measurement of S100B release by ELISA assay. (D) Analysis of GFAP and S100B protein expression by immunofluorescence (magnification 10 × ). Results are the mean ± S.E.M. of n = 4 separate experiments. ***P < 0.001 versus control; ###P < 0.01 versus Aβ-challenged cells; °°°P < 0.001 and °P < 0.05 versus Aβ+ PEA-challenged cells.
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Related In: Results  -  Collection

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

fig01: PEA attenuates Aβ-induced astrocyte activation. 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). GFAP mRNA was evaluated 12 hrs following Aβ challenge; GFAP and S100B protein expression was evaluated after 24 hrs of treatments by Western blot and immunofluorescence analyses. S100B release in the cellular milieu was determined 24 hrs after Aβ challenge by ELISA assay. (A) Results of GFAP and S100B Western blot analysis and densitometric analysis of corresponding bands. β-actin was used as loading control. (B) Results of GFAP RT-PCR amplification and densitometric analysis of corresponding bands. GAPDH was used as standard control. (C) Measurement of S100B release by ELISA assay. (D) Analysis of GFAP and S100B protein expression by immunofluorescence (magnification 10 × ). Results are the mean ± S.E.M. of n = 4 separate experiments. ***P < 0.001 versus control; ###P < 0.01 versus Aβ-challenged cells; °°°P < 0.001 and °P < 0.05 versus Aβ+ PEA-challenged cells.
Mentions: In order to test the effect of PEA on Aβ-induced astrogliosis, the expression of GFAP and S100B, specific markers of astrocyte activity, was explored. Reactive astrocytes display hypertrophied cell bodies and thickened processes exhibiting GFAP-immunoreactivity. Using immunofluorescence, Western blot and RT-PCR analyses, we observed a marked increase in both transcription and expression of GFAP after Aβ challenge. This enhancement was significantly attenuated by PEA treatment. Moreover, the PPAR-α antagonist MK886 was able to partly blunt the PEA-induced attenuation of GFAP transcription and expression. Such effect indicated a significant, although not exclusive, involvement of the PPAR-α receptor in mediating PEA action (Fig. 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