PALMITOYLETHANOLAMIDE: ANTI-INFLAMMATORY AGENT AND A GUARD AGAINST INFLUENZA AND COMMON COLD

Palmitoylethanolamide (PEA) is a meal element acknowledged for longer than 50 years. PEA is amalgamated and metabolized by various animal cell samples and also existing in plants. It exerts a multitude of physiological functions related to metabolic and cellular homeostasis. PEA was previously recognized in the 50s of the latest era as a therapeutic element with potent anti-inflammatory characteristics.

Since 1970, the anti-inflammatory and additional immune-modulating features of PEA have been manifested in several placebo-controlled double-blind clinical experiments on influenza and the usual cold. Positive results coincided with the clinical use of PEA in former Czechoslovakia under the brand name Impulsion.

ANTI-INFLAMMATORY MECHANISM AND ACTION (APPLICATION) OF PALMITOYLETHANOLAMIDE

MECHANISM:

  • In an artistic research on the anti-inflammatory and pro-apoptotic motions of anandamide, it was revealed that it can hinder tumor necrosis factor-α-induced NF-κB activation [18]. The NF-κB inhibitory activity of anandamide was independent of CB1 and CB2. Structure-activity relationships demonstrated that analogs with saturated fatty acyl groups were more active than unsaturated analogs. Saturated acylethanolamines such as PEA, therefore, offer a new opportunity to modify chronic inflammation in autoimmune disorders.

  • Starting with Professor Rita Levi-Montalcini’s work, it became clear that PEA regulates many pathophysiological processes, and PEA has since been found to be effective in a number of animal models for inflammation, neuroinflammation, neurotoxicity, and chronic pain. Levi-Montalcini highlighted the importance of activation of inflammatory cascades via the activation of nonneuronal cells, such as mast cells.

ACTION (APPLICATION):

  • Micronized and ultra-micronized PEA possessed superior pharmacological action against carrageenan-induced inflammatory pain, in contrast to the preparation of non-micronized PEA, which failed to show efficacy when orally given in this model. The anti-inflammatory action of PEA combined with an antioxidant could potentiate its pharmacological effects. Amidst the essential molecules that can neutralize the peroxidation processes, there are numerous flavonoids, such as Luteolin, Polydatin, Quercetin, and Silymarin, which hold different pharmacological conclusions and treatments.
  • A mixture of PEA and Baicalein has been latterly investigated in a myocardial I/R damage type. In this study, treatment with PEA-Baicalein was shown to reduce myocardial tissue injury, neutrophil infiltration, markers for expression of mast cell activation, such as chymase and tryptase, and pro-inflammatory cytokine production (TNF-α and IL-1β). Moreover, operation with PEA-Baicalein decreased nitrotyrosine and PAR configuration, repressed NF-kB nuclear translocation, and accentuated apoptosis pathways.

FINAL CONCLUSION:

PEA is a universal material provided by the body and discovered in numerous foods. It is not an opioid or addictive. Preparatory readings designate that PEA does not advance pharmacological toleration or progressively fall effectiveness over time as happens with opioids.

It is harmless for patients with no recorded serious side impacts like Pterostilbene and it is contemplated to lack intense or chronic toxicity. It does not meddle with other vaccination therapies nor does it trigger drug-drug communications.

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