Effects of palmitoylethanolamide on release of mast cell peptidases and neurotrophic factors after spinal cord injury

@article{Esposito2011EffectsOP,
  title={Effects of palmitoylethanolamide on release of mast cell peptidases and neurotrophic factors after spinal cord injury},
  author={Emanuela Esposito and Irene Paterniti and Emanuela Mazzon and Tiziana Genovese and Rosanna Di Paola and Maria Galuppo and Salvatore Cuzzocrea},
  journal={Brain, Behavior, and Immunity},
  year={2011},
  volume={25},
  pages={1099-1112}
}
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89 Citations
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89 Citations

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Palmitoylethanolamide in homeostatic and traumatic central nervous system injuries.
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An overview of current knowledge of PEA effect on glial functions in the brain and how targeting glial-specific pathways might ultimately impact the development of therapies for clinical management of neurodegenerative disorders is provided.
Administration of palmitoylethanolamide (PEA) protects the neurovascular unit and reduces secondary injury after traumatic brain injury in mice
The Association of Palmitoylethanolamide with Luteolin Decreases Autophagy in Spinal Cord Injury
TLDR
Results showed that treatment with co-ultraPEALut after SCI reduced the expression of proteins promoter of autophagy such as Beclin-1 and microtubule-associated protein 1A/1B-light chain 3 (MAP-LC3) and could be considered as a possible therapeutic approach in an acute traumatic lesion like SCI.
The association of adelmidrol with sodium hyaluronate displays beneficial properties against bladder changes following spinal cord injury in mice
TLDR
Data show the protective roles of adelmidrol + sodium hyaluronate on bladder following SCI, highlighting a potential therapeutic target for the reduction of bladder changes.
The neuroprotective effects of micronized PEA (PEA‐m) formulation on diabetic peripheral neuropathy in mice
TLDR
It is demonstrated that PEA‐m represents a new therapeutic strategy for neuroinflammation pain associated with mixed neuropathies and could be correlated at least in part to peroxisome proliferator‐activated receptor‐α activation.
A new co-ultramicronized composite including palmitoylethanolamide and luteolin to prevent neuroinflammation in spinal cord injury
TLDR
The present study demonstrates that the protective effect of PEA on SCI-associated neuroinflammation could be improved by co-ultramicronization with Lut possibly due to its antioxidant properties.
Co-Ultramicronized Palmitoylethanolamide/Luteolin Promotes Neuronal Regeneration after Spinal Cord Injury
TLDR
Findings show a prominent effect of co-ultraPEALut administration in the management of survival and differentiation of new neurons and spine maturation, and may represent a therapeutic treatment for spinal cord and other traumatic diseases.
PEA and luteolin synergistically reduce mast cell-mediated toxicity and elicit neuroprotection in cell-based models of brain ischemia
N-Palmitoylethanolamine and Neuroinflammation: a Novel Therapeutic Strategy of Resolution
TLDR
The role of mast cells and glia in neuroinflammation and strategies to modulate their activation based on leveraging natural mechanisms with the capacity for self-defense against inflammation are discussed.
Non-neuronal cell modulation relieves neuropathic pain: efficacy of the endogenous lipid palmitoylethanolamide.
TLDR
The data show that PEA delayed mast cell recruitment, protected mast cells against degranulation and abolished the nerve growth factor increase in sciatic nerve concomitantly preserving the nerve from degeneration, while reducing microglia activation in the spinal cord.
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References

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TLDR
It is indicated that PEA reduces inflammation and tissue injury associated with SCI and suggest a regulatory role for endogenous PPAR-α signaling in the inflammatory response associated with spinal cord trauma.
Poly(ADP-Ribose) Glycohydrolase Activity Mediates Post-Traumatic Inflammatory Reaction after Experimental Spinal Cord Trauma
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The results indicate that PARG activity modulates the inflammatory response and tissue injury events associated with spinal cord trauma and participate in target organ damage under these conditions.
The endocannabinoid system is modulated in response to spinal cord injury in rats
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