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1.
Figure 3

Figure 3. Effects of elmiric acids in the mouse subcutaneous pouch assay. From: The elmiric acids: biologically active anandamide analogs.

The data shown were previously reported in . P<0.05 by ANOVA vs. the oil control.
Note: see for structures.

Sumner Burstein. Neuropharmacology. ;55(8):1259-1264.
2.
Figure 4

Figure 4. Effects of elmiric acids on ear edema compared with increases in prostaglandin ratio. From: The elmiric acids: biologically active anandamide analogs.

The data presented here were previously reported in . The values shown in this comparison represent the maximum response in each case.
Note: EMA-1 = glycine; EMA-2 = alanine; EMA-22 = 1,1-dimethylglycine; EMA-25 = 1-amino-cyclohexane-carboxylic acid.
*i = immunoreactive.

Sumner Burstein. Neuropharmacology. ;55(8):1259-1264.
3.
Figure 2

Figure 2. Effects of elmiric acids on the ratio of iPGJ/iPGE* in RAW cell media. From: The elmiric acids: biologically active anandamide analogs.

The data shown were previously reported in . All of the ratio values greater than 20 are significant at the 95% confidence level when compared to the DMSO-LPS control by ANOVA.
Note: see for structures.
*i denotes immunoreactive.

Sumner Burstein. Neuropharmacology. ;55(8):1259-1264.
4.
Figure 1

Figure 1. Effects of elmiric acids on the proliferation of mouse macrophage RAW cells. From: The elmiric acids: biologically active anandamide analogs.

The data shown were previously reported in . The cells were treated with 1 and 10 uM elmiric acid whose identity is shown on the Y axis (designated as 1 or 10 on the Y axis). Luminometer units are directly proportional to the number of metabolically active cells and are a measure of ATP levels.

Sumner Burstein. Neuropharmacology. ;55(8):1259-1264.
5.
Figure 5

Figure 5. EMA-1 (20:4) – induced stimulation of arachidonic acid release from RAW cells (Burstein, unpublished findings). From: The elmiric acids: biologically active anandamide analogs.

Cells were grown and maintained as described previously (). Following a 2 hr labeling period with 14C-arachidonic acid, the media (RPMI+0.1% BSA) were changed and the cells treated for 1 hr with EMA-1 (20:4) in 10 ul of DMSO. The control was 10 ul of DMSO and there were 4 replicates of each treatment concentration. Release was measured by liquid scintillation counting on a 0.1 ml aliquot of medium. Values shown are the means (∓) SD.
Note: The cells were treated with non-radioactive EMA-1 (20:4).

Sumner Burstein. Neuropharmacology. ;55(8):1259-1264.
6.
Figure 6

Figure 6. Putative mechanism for the anti-inflammatory actions of the elmiric acids. From: The elmiric acids: biologically active anandamide analogs.

Induction of inflammation. A wide range of pro inflammatory agonists can activate various forms of phospholipase A2 causing the release of free arachidonic acid from pools of phospholipids. Several routes of regulated biotransformation can then lead to elevated levels of various mediators of inflammation.
Resolution by elmiric acids. An elmiric acid, activating a receptor, promotes the mobilization of Ca++ that in turn causes the release of free arachidonic acid. COX-2 action then results in the production of PGG2 and PGH2 that is converted by a terminal synthetase to PGD2. In a non-enzymic process, PGD2 is transformed into 15-deoxy-PGJ2, a potent anti inflammatory mediator.

Sumner Burstein. Neuropharmacology. ;55(8):1259-1264.

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