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Akhilesh Kumar, Zhuanhong Qiao, Pritesh P. Kumar, Zhao-Hui Song; Effect of Oleoylethanolamide on Aqueous Humor Outflow. Invest. Ophthalmol. Vis. Sci. 2012;53(14):1989.
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To study the effects of oleoylethanolamide (OEA) on aqueous humor outflow via the trabecular meshwork pathway.
The effects of OEA on aqueous humor outflow via the trabecular meshwork pathway were measured using a porcine anterior segment perfused organ culture model. Different concentrations of OEA were administered to the perfusion medium and the aqueous humor outflow facility was monitored for 5 hours. SR141716A, SR144528, O-1918, and GW6471 were administered to anterior segment to determine the involvement of various receptors on the outflow effects of OEA. PD98059, an inhibitor of the p42/44 MAP kinase pathway , was used to examine the involvement of the MAP kinase signal transduction pathway in regulating OEA induced enhancement of outflow facility. OEA induced activation of p42/44 MAP kinase was determined by western blot analysis using an anti-phospho p42/44 MAP kinase antibody.
Administration of OEA caused a concentration-dependent enhancement of aqueous humor outflow facility, with the maximum effect (162.4 ± 15.3 % of basal outflow facility) achieved at 2 hour after the administration of 30 nM of OEA. Pretreatment with either 1 µM SR144528 or 3 µM GW6471 produced a partial antagonism on the OEA-induced increased aqueous humor outflow facility. However, pretreatment with either 1 µM O-1918 or 1 µM SR141716A had no effect on OEA induced enhancement of aqueous humor outflow facility. Treatment of trabecular meshwork cells with OEA for 10 min activated phosphorylation of p42/44 MAP kinase, which was blocked by pretreatment with either GW6471 or SR144528. Furthermore, PD98059, an inhibitor of the p42/44 MAP kinase pathway, blocked both OEA-induced phosphorylation of p42/44 MAP kinase and enhancement of aqueous humor outflow facility.
The results from this study demonstrate that OEA increases aqueous humor outflow through the trabecular meshwork pathway and these effects may be mediated by PPARα and non-CB1/CB2 cannabinoid receptors through activation of p42/44 MAP kinase.
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