April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Effect of Palmitylethanolamide on Aqueous Humor Outflow
Author Affiliations & Notes
  • Akhilesh Kumar
    Pharmacology & Toxicology, University of Louisville, Louisville, Kentucky
  • Zhuanhong Qiao
    Pharmacology & Toxicology, University of Louisville, Louisville, Kentucky
  • Pritesh Kumar
    Pharmacology & Toxicology, University of Louisville, Louisville, Kentucky
  • Zhao-Hui Song
    Pharmacology & Toxicology, University of Louisville, Louisville, Kentucky
  • Footnotes
    Commercial Relationships  Akhilesh Kumar, None; Zhuanhong Qiao, None; Pritesh Kumar, None; Zhao-Hui Song, None
  • Footnotes
    Support  NIH Grants EY13632 and DA11551
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 1524. doi:https://doi.org/
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      Akhilesh Kumar, Zhuanhong Qiao, Pritesh Kumar, Zhao-Hui Song; Effect of Palmitylethanolamide on Aqueous Humor Outflow. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1524. doi: https://doi.org/.

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Abstract

Purpose: : To study the effects of palmitoylethanolamide (PEA), a fatty acid ethanolamide and an endogenous cannabinoid, on aqueous humor outflow via the trabecular meshwork pathway.

Methods: : The effects of PEA on aqueous humor outflow via the trabecular meshwork pathway were measured using a porcine anterior segment perfused organ culture model. Different concentrations of PEA were administered to the perfusion medium and the aqueous humor outflow facility was monitored for 5 hours. CB1 antagonist SR141716A and CB2 antagonist SR144528 were used, respectively, to investigate the possible involvement of CB1 and CB2 receptors in the outflow effects induced by PEA. O-1918, a cannabidiol analog that acts as a selective antagonist at the non-CB1/CB2 receptors, was also used to investigate whether non-CB1/CB2 cannabinoid receptors are involved in the PEA-induced outflow effects. PEA induced activation of p42/44 mitogen-activated protein (MAP) kinase was determined by western blot analysis using an anti-phospho p42/44 MAP kinase antibody.

Results: : Administration of PEA caused a concentration-dependent enhancement of aqueous humor outflow facility, with the maximum effect (135.6 ± 7.1 % of basal outflow facility) achieved at 2 hour after the administration of 30 nM of PEA. Pretreatment with 1 µM O-1918 produced a full antagonism on the PEA-induced increase of aqueous humor outflow facility. However, pretreatment with 1µM of SR141716A or 1µM of SR141716A had no effect on PEA-induced enhancement of aqueous humor outflow facility. Treatment of trabecular meshwork cells with PEA for 10 min activated phosphorylation of p42/44 MAP kinase which was blocked by pretreatment with O-1918. Furthermore, PD98059, an inhibitor of the p42/44 MAP kinase pathway, blocked both PEA-induced phosphorylation of p42/44 MAP kinase and enhancement of aqueous humor outflow facility.

Conclusions: : The results from this study demonstrate that PEA increases aqueous humor outflow through the trabecular meshwork pathway, and these effects are mediated by non-CB1/CB2 cannabinoid receptors through activation of p42/44.

Keywords: intraocular pressure • anterior segment • aqueous 
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