Palmitoylethanolamide Stimulation Induces Allopregnanolone Synthesis in C6 Cells and Primary Astrocytes: Involvement of Peroxisome‐Proliferator Activated Receptor‐α

@article{Raso2011PalmitoylethanolamideSI,
  title={Palmitoylethanolamide Stimulation Induces Allopregnanolone Synthesis in C6 Cells and Primary Astrocytes: Involvement of Peroxisome‐Proliferator Activated Receptor‐$\alpha$},
  author={Giuseppina Mattace Raso and Emanuela Esposito and Sergio Vitiello and Anna Iacono and Anna Santoro and Giuseppe D'Agostino and Oscar Sasso and Roberto Russo and P. V. Piazza and Antonio Calignano and Rosaria Meli},
  journal={Journal of Neuroendocrinology},
  year={2011},
  volume={23}
}
Palmitoylethanolamide (PEA) regulates many pathophysiological processes in the central nervous system, including pain perception, convulsions and neurotoxicity, and increasing evidence points to its neuroprotective action. In the present study, we report that PEA, acting as a ligand of peroxisome‐proliferator activated receptor (PPAR)‐α, might regulate neurosteroidogenesis in astrocytes, which, similar to other glial cells and neurones, have the enzymatic machinery for neurosteroid de novo… 
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TLDR
This review mobilizes a considerable number of findings that discuss miscellaneous axes, covering the detailed expression pattern of PPARα in species and tissues, the lessons from several PPAR α KO mouse models and the modulation ofPPARα function by dietary micronutrients.
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Allopregnanolone attenuates Aβ25-35-induced neurotoxicity in PC12 cells by reducing oxidative stress.
  • X. Qian, H. Cao, Jun Li
  • Biology, Chemistry
    International journal of clinical and experimental medicine
  • 2015
TLDR
It is demonstrated that Allopregnano-lone (APα), a neurosteroid derive from neuroactive progesterone, exerts a protective effect against Aβ25-35-induced neurotoxicity in PC12 cells.
Neuroprotective Activities of Palmitoylethanolamide in an Animal Model of Parkinson's Disease
TLDR
Chronic treatment with palmitoylethanolamide (PEA) protects against MPTP-induced neurotoxicity and the ensuing functional deficits even when administered once the insult has been initiated, and chronic PEA reversedMPTP-associated motor deficits.
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