N-(2-hydroxyethyl)hexadecanamide is orally active in reducing edema formation and inflammatory hyperalgesia by down-modulating mast cell activation

Eur J Pharmacol. 1996 Apr 11;300(3):227-36. doi: 10.1016/0014-2999(96)00015-5.

Abstract

Mast cells play a key role in inflammatory reactions triggered by tissue injury or immune perturbations. Little is known about endogenous molecules and mechanisms capable of modulating inappropriate mast cell activity. N-(2-Hydroxyethyl)hexadecanamide (palmitoylethanolamide), found in peripheral tissues, has been proposed to act as a local autacoid capable of negatively regulating mast cell activation and inflammation-hence the acronym Autacoid Local Inflammation Antagonism (ALIA). Recently, N-(2-hydroxyethyl)hexadecanamide (LG 2110/1) has been reported to down-modulate mast cell activation in vitro by behaving as an agonist at the peripheral cannabinoid CB2 receptor. Here, we have characterized and functionally correlated the anti-inflammatory actions of LG 2110/1 with its ability to control mast cell activation, when given orally in a battery of rodent models of inflammation. LG 2110/1 diminished, in a dose-dependent and correllated manner, the number of degranulated mast cells and plasma extravasation induced by substance P injection in the mouse ear pinna. In addition, LG 2110/1 reduced dose dependently plasma extravasation induced by passive cutaneous anaphylaxis reaction. In adult rats LG 2110/1 decreased, in a dose-dependent manner, carrageenan-induced hindpaw edema and hyperalgesia, but not phospholipase A2-induced hindpaw edema. Further, anti-edema effects were observed when utilizing dextran and formalin, known to also cause mast cell activation. Locally administered LG 2110/1 was likewise effective in minimizing dextran-induced hind paw edema. In contrast, equivalent amounts of palmitic acid plus ethanolamine were ineffective against plasma extravasation provoked by substance P. LG 2110/1 did not decrease plasma extravasation induced by the substance P fragment, substance P-(6-11), known to be inactive on mast cells. These results indicate that orally administered N-(2-hydroxyethyl)hexadecanamide is effective in: (a) directly down-modulating mast cell activation in vivo; (b) suppressing pathological consequences initiated by mast cell activation independently of the activating stimuli; (c) exerting an anti-inflammatory action distinguishable from that of classical steroidal and non-steroidal anti-inflammatory agents. These findings raise the possibility that N-(2-hydroxyethyl)hexadecanamide and related saturated N-acylamides ('ALIAmides') represent novel therapeutic agents useful in the management of inflammatory disease conditions.

MeSH terms

  • Amides
  • Analysis of Variance
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Carrageenan
  • Cell Degranulation
  • Dextrans
  • Ear, External / physiology
  • Edema / chemically induced
  • Edema / prevention & control*
  • Endocannabinoids
  • Ethanolamines
  • Evans Blue
  • Excipients
  • Extravasation of Diagnostic and Therapeutic Materials / drug therapy
  • Female
  • Formaldehyde
  • Hyperalgesia / chemically induced
  • Hyperalgesia / prevention & control*
  • Male
  • Mast Cells / drug effects*
  • Mast Cells / metabolism
  • Mast Cells / physiology
  • Mice
  • Mice, Inbred BALB C
  • Palmitic Acids / pharmacology*
  • Passive Cutaneous Anaphylaxis
  • Rats
  • Rats, Wistar
  • Substance P / administration & dosage
  • Substance P / pharmacology*

Substances

  • Amides
  • Anti-Inflammatory Agents, Non-Steroidal
  • Dextrans
  • Endocannabinoids
  • Ethanolamines
  • Excipients
  • Palmitic Acids
  • Formaldehyde
  • Substance P
  • Evans Blue
  • palmidrol
  • Carrageenan