Wikipedia

Stearoylethanolamide

Stearoylethanolamide (SEA) is an endocannabinoid neurotransmitter.[1]

Stearoylethanolamide
Names
IUPAC name
N-(2-Hydroxyethyl)octadecanamide
Identifiers
3D model (JSmol)
ChemSpider
ECHA InfoCard 100.003.531 Edit this at Wikidata
UNII
  • InChI=1S/C20H41NO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-20(23)21-18-19-22/h22H,2-19H2,1H3,(H,21,23)
    Key: OTGQIQQTPXJQRG-UHFFFAOYSA-N
  • CCCCCCCCCCCCCCCCCC(=O)NCCO
Properties
C20H41NO2
Molar mass 327.553 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

Stearoylethanolamide (C20H41NO2; 18:0), also called N-(octadecanoyl)ethanolamine, is an endogenously formed N-acylethanolamine (NAE) and the ethanolamide of octadecanoic acid (C18H36O2; 18:0) and ethanolamine (MEA: C2H7NO), and functionally related to an octadecanoic acid.[2][3] SEA is produced by the phospholipase D hydrolysis of membrane phospholipids.[4]

Within the class of NAEs, SEA is among anandamide, a major endocannibonoid that binds to CB1 and CB2, found in the brain and immune system, respectively.[5] SEA, however, does not display any signs of binding to CB1/CB2 receptors, yet still has cannabimimetic activity.[3]

Levels of SEA correlate with changes in pain intensity, indicating this SEA change, reflect the pain reduction effects of IPRP.[6]

Role in Neuroprotection

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Neuroinflammation is triggered by a variety of neurodegenerative disorders and inflammatory conditions like infections, traumatic brain injury, and stress.[3] Systemic inflammation can significantly alter blood–brain barrier (BBB) permeability via allowing infiltration by immune cells and causing structural damage to the glycocalyx.[7]

SEA acts as a protective agent against this; it can result in a slower onset and also contribute to faster resolution of damage.[3] One way in which SEA can do so is through lowering glutamate levels in the prefrontal cortex, which increases when inflamed.[3] A high flow of glutamate results in greater recruitment of microglia to neurons, furthering the inflammatory response. With SEA, this cycle is interrupted and thus the initial neuroinflammatory state is dampened by keeping glutamate levels low.[3] Another mechanism by which SEA acts a neuroprotective agent is through increasing 2-AG levels in the brain, which allows for smoother inflammatory response resolution.[3]

Role in Chronic Pain

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Chronic pain is defined as persistent or recurring pain lasting longer than three months, going past the typical healing period of injury.[8] NAEs, like SEA, play a role in remediating this inflammation, evidenced through their elevated levels during periods of pain.[9]

A proposed mechanism of SEA function is as an agonist of the peroxisome proliferator-activated receptor gamma (PPARγ), competing against the antagonist GW9662 and agonist LY-171883, and overall contributing anti-inflammatory activity.[10][11] SEA also has been shown to inhibit NF-κB activity, via blocking its translocation into the nuclei of macrophages by Lipopolysaccharide, and thereby suppressing pro-inflammatory cytokine production.[12]

References

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  1. ↑ Mauro Maccarrone, Riccardo Pauselli, Marianna Di Rienzo, Alessandro Finazzi-Agrò (2002). "Binding, degradation and apoptotic activity of stearoylethanolamide in rat C6 glioma cells". Biochem J. 366 (Pt 1): 137–144. doi:10.1042/BJ20020438. PMC 1222758. PMID 12010121.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. ↑ PubChem. "N-(2-Hydroxyethyl)octadecanamide". pubchem.ncbi.nlm.nih.gov. Retrieved 2022-09-27.
  3. 1 2 3 4 5 6 7 Kasatkina, Ludmila A.; Heinemann, Akos; Hudz, Yehor A.; Thomas, Dominique; Sturm, Eva M. (2020-04-01). "Stearoylethanolamide interferes with retrograde endocannabinoid signalling and supports the blood-brain barrier integrity under acute systemic inflammation". Biochemical Pharmacology. 174 113783. doi:10.1016/j.bcp.2019.113783. ISSN 0006-2952. PMID 31881191.
  4. ↑ Di MARZO, Vincenzo; De PETROCELLIS, Luciano; Sepe, Nunzio; Buono, Anna (1996-06-15). "Biosynthesis of anandamide and related acylethanolamides in mouse J774 macrophages and N18 neuroblastoma cells". Biochemical Journal. 316 (3): 977–984. doi:10.1042/bj3160977. ISSN 0264-6021. PMC 1217444. PMID 8670178.
  5. ↑ Simankowicz, Paulina; Stępniewska, Joanna (2025-04-21). "The Role of Endocannabinoids in Physiological Processes and Disease Pathology: A Comprehensive Review". Journal of Clinical Medicine. 14 (8): 2851. doi:10.3390/jcm14082851. ISSN 2077-0383. PMC 12027566. PMID 40283681.
  6. ↑ Stensson, Niclas; Gerdle, Björn; Rönne-Petersén, Linn; Yang, Liu L.; Lavebratt, Catharina; Falkenberg, Torkel; Ghafouri, Bijar (2022-02-26). "Investigating the Long-Term Effect of an Interdisciplinary Multimodal Rehabilitation Program on Levels of Bioactive Lipids and Telomerase Activity in Blood from Patients with Chronic Pain". Journal of Clinical Medicine. 11 (5): 1291. doi:10.3390/jcm11051291. ISSN 2077-0383. PMC 8911430. PMID 35268382.
  7. ↑ Galea, Ian (November 2021). "The blood–brain barrier in systemic infection and inflammation". Cellular & Molecular Immunology. 18 (11): 2489–2501. doi:10.1038/s41423-021-00757-x. ISSN 2042-0226. PMC 8481764. PMID 34594000.
  8. ↑ Rikard, S. Michaela; Strahan, Andrea E.; Schmit, Kristine M.; Guy, Gery P. (2023-04-14). "Chronic Pain Among Adults — United States, 2019–2021". MMWR. Morbidity and Mortality Weekly Report. 72 (15): 379–385. doi:10.15585/mmwr.mm7215a1. ISSN 0149-2195. PMC 10121254. PMID 37053114.
  9. ↑ Ghafouri, Nazdar; Ghafouri, Bijar; Larsson, Britt; Stensson, Niclas; Fowler, Christopher J.; Gerdle, Björn (September 2013). "Palmitoylethanolamide and stearoylethanolamide levels in the interstitium of the trapezius muscle of women with chronic widespread pain and chronic neck-shoulder pain correlate with pain intensity and sensitivity". Pain. 154 (9): 1649–1658. doi:10.1016/j.pain.2013.05.002. ISSN 0304-3959. PMID 23707281.
  10. ↑ Stensson, Niclas; Ghafouri, Nazdar; Ernberg, Malin; Mannerkorpi, Kaisa; Kosek, Eva; Gerdle, Björn; Ghafouri, Bijar (November 2018). "The Relationship of Endocannabinoidome Lipid Mediators With Pain and Psychological Stress in Women With Fibromyalgia: A Case-Control Study". The Journal of Pain. 19 (11): 1318–1328. doi:10.1016/j.jpain.2018.05.008. ISSN 1526-5900. PMID 29885369.
  11. ↑ Kosiakova, H.; Berdyshev, A.; Dosenko, V.; Drevytska, T.; Herasymenko, O.; Hula, N. (November 2022). "The involvement of peroxisome proliferator-activated receptor gamma (PPARγ) in anti-inflammatory activity of N-stearoylethanolamine". Heliyon. 8 (11) e11336. Bibcode:2022Heliy...811336K. doi:10.1016/j.heliyon.2022.e11336. ISSN 2405-8440. PMC 9641209. PMID 36387464.
  12. ↑ Kosiakova, H.; Berdyshev, A.; Dosenko, V.; Drevytska, T.; Herasymenko, O.; Hula, N. (November 2022). "The involvement of peroxisome proliferator-activated receptor gamma (PPARγ) in anti-inflammatory activity of N-stearoylethanolamine". Heliyon. 8 (11) e11336. Bibcode:2022Heliy...811336K. doi:10.1016/j.heliyon.2022.e11336. ISSN 2405-8440. PMC 9641209. PMID 36387464.


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