N-Arachidonoyl dopamine

Source: Wikipedia, the free encyclopedia.
N-Arachidonoyl dopamine
Names
Preferred IUPAC name
(5Z,8Z,11Z,14Z)-N-[2-(3,4-Dihydroxyphenyl)ethyl]icosa-5,8,11,14-tetraenamide
Other names
NADA
Identifiers
3D model (
JSmol
)
ChEMBL
ChemSpider
IUPHAR/BPS
  • InChI=1S/C28H41NO3/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-28(32)29-23-22-25-20-21-26(30)27(31)24-25/h6-7,9-10,12-13,15-16,20-21,24,30-31H,2-5,8,11,14,17-19,22-23H2,1H3,(H,29,32)/b7-6-,10-9-,13-12-,16-15- checkY
    Key: MVVPIAAVGAWJNQ-DOFZRALJSA-N checkY
  • InChI=1/C28H41NO3/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-28(32)29-23-22-25-20-21-26(30)27(31)24-25/h6-7,9-10,12-13,15-16,20-21,24,30-31H,2-5,8,11,14,17-19,22-23H2,1H3,(H,29,32)/b7-6-,10-9-,13-12-,16-15-
    Key: MVVPIAAVGAWJNQ-DOFZRALJBM
  • CCCCC\C=C/C\C=C/C\C=C/C\C=C/CCCC(=O)NCCC1=CC(=C(C=C1)O)O
Properties
C28H41NO3
Molar mass 439.63 g/mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

N-Arachidonoyl dopamine (NADA) is an

endogenous TRPV1 agonist.[2]

In mice, NADA was shown to induce the tetrad of physiological paradigms associated with cannabinoids: hypothermia, hypo-locomotion, catalepsy, and analgesia.[1][3][4] NADA has been found to play a regulatory role in both the peripheral and central nervous systems, and displays antioxidant and neuroprotectant properties.[2][5][6][7] NADA has also been implicated in smooth muscle contraction and vasorelaxation in blood vessels.[8][9][10][11] Additionally, NADA has been observed to suppress inflammatory activation of human Jurkat T cells and to inhibit the release of prostaglandin E2 (PGE2) from lipopolysaccharide (LPS)-activated astrocytes, microglia and mouse brain ECs (MEC-Brain).[12][13][14] NADA also promotes the inflammatory resolution of human endothelial cells activated by both endogenous (i.e. TNF) and exogenous (i.e. bacterial derived LPS (TLR4 agonist) and FSL-1 (TLR2/6 agonist)) inflammatory mediators.[15] It can increase the TRPV1-mediated release of substance P and calcitonin gene-related peptide (CGRP) in rat dorsal spinal cord slices.[2] Furthermore, NADA also displays inhibitory activity in HIV-1 replication assays.[16] Finally, NADA can prevent the degranulation and release of TNF from RBL- 2H3 mast cells treated with an IgE-antigen complex.[17] Together, these studies show that physiological functions attributed to NADA are multifaceted, and include the ability to modulate the immune response.

The biosynthetic pathway of N-arachindonoyldopamine is not well understood. It has been proposed to be conjugated from arachidonoyl-CoA or arachidonoyl phospholipids and dopamine, but in vitro experiments do not support this theory.[18] However, the indirect biosynthesis of phospholipid esters with dopamine may be possible, as dopamine can induce the aminolysis of the glycerol-fatty acid bonds in phospholipid chains (arachidonoyl, palmitoyl, linoleyl, etc.).[19]

See also

  • Endocannabinoid

References

  1. ^
    PMID 11042139
    .
  2. ^
    PMID 12060783
    .
  3. PMID 11229744
    .
  4. PMID 2849657
    .
  5. PMID 15006899
    .
  6. PMID 16760924
    .
  7. S2CID 42626601
    .
  8. S2CID 23436811
    .
  9. PMID 12954366
    .
  10. PMID 14769783
    .
  11. PMID 19421417
    .
  12. S2CID 205620351
    .
  13. PMID 20206142
    .
  14. PMID 14764703
    .
  15. PMID 24644287
    .
  16. PMID 16148147
    .
  17. S2CID 3995567
    .
  18. PMID 19570666
    .
  19. PMID 6726084
    . Retrieved 2017-12-15.

External links
Retrieved from "https://en.wikipedia.org/w/index.php?title=N-Arachidonoyl_dopamine&oldid=1170978730"