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Arachidonic Acid methyl ester Sale

(Synonyms: 花生四烯酸甲酯) 目录号 : GC41392

An esterified form of arachidonic acid

Arachidonic Acid methyl ester Chemical Structure

Cas No.:2566-89-4

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产品描述

Arachidonic acid is the keystone essential fatty acid at the origin of the arachidonic acid cascade. It is converted by cyclooxygenase, lipoxygenase, and epoxygenase enzymes into more than one hundred fifty different potent primary autacoid metabolites in species ranging from fungi to plants to mammals. Arachidonic acid is stored in tissue phospholipids in esterified form, where it comprises a small but critically controlled percentage of the polyunsaturated fatty acid pool. Arachidonic acid content is frequently measured by the saponification of the lipid fraction followed by methyl esterification and gas chromatographic analysis of the resulting FAME (fatty acid methyl ester) compounds. Arachidonic acid methyl ester can also be incorporated into dietary regimens or fed to cultured cells as a source of exogenous arachidonate.

Chemical Properties

Cas No. 2566-89-4 SDF
别名 花生四烯酸甲酯
Canonical SMILES CCCCC/C=C\C/C=C\C/C=C\C/C=C\CCCC(OC)=O
分子式 C21H34O2 分子量 318.5
溶解度 DMF: miscible,DMSO: miscible,Ethanol: miscible 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 3.1397 mL 15.6986 mL 31.3972 mL
5 mM 0.6279 mL 3.1397 mL 6.2794 mL
10 mM 0.314 mL 1.5699 mL 3.1397 mL
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Research Update

Arachidonic acid increases c-fos and Egr-1 mRNA in 3T3 fibroblasts by formation of prostaglandin E2 and activation of protein kinase C

J Biol Chem 1994 Nov 4;269(44):27258-63.PMID:7961634doi

Studying Swiss 3T3 fibroblasts, we report that arachidonic acid strongly stimulates mRNA levels of the growth-associated immediate early genes c-fos and Egr-1. Structurally related compounds like Arachidonic Acid methyl ester, arachidonyl alcohol, or eicosatetraynoic acid are ineffective, indicating a specific role of free unesterified arachidonic acid or an arachidonic acid metabolite in c-fos and Egr-1 mRNA accumulation. Blocking the conversion of arachidonic acid to prostaglandins by inhibiting cyclooxygenase abolishes arachidonic acid-induced accumulation of c-fos and Egr-1 mRNA. Inhibition of the lipoxygenase or cytochrome P-450 epoxygenase pathways has no significant effect on arachidonic acid-induced c-fos and Egr-1 mRNA levels, indicating that prostaglandin synthesis is necessary for the increase in c-fos and Egr-1 mRNA. Reversed phase high performance liquid chromatography revealed prostaglandin E2 (PGE2) as the major arachidonic acid metabolite in Swiss 3T3 fibroblasts. When added to the cells, PGE2 stimulates c-fos and Egr-1 mRNA levels to the same degree as arachidonic acid. Also, the inhibition of arachidonic acid-stimulated c-fos and Egr-1 mRNA accumulation by indomethacin is reversed by PGE2. Contrary to reports that PGE2 caused an increase in cAMP levels in Swiss 3T3 fibroblasts, we found that arachidonic acid and PGE2 only minimally increase cAMP levels as compared with untreated cells. In contrast, inhibition of protein kinase C by calphostin C and chelerythrine or down-regulation with phorbol 12-myristate 13-acetate drastically reduces PGE2 and arachidonic acid-induced c-fos and Egr-1 mRNA levels. These data indicate that arachidonic acid exerts its stimulatory effect on c-fos and Egr-1 mRNA via synthesis of PGE2 and subsequent activation of protein kinase C, probably through a PGE2 receptor coupled to phospholipase C.

Inhibition of C6 glioma cell proliferation by anandamide, 1-arachidonoylglycerol, and by a water soluble phosphate ester of anandamide: variability in response and involvement of arachidonic acid

Biochem Pharmacol 2003 Sep 1;66(5):757-67.PMID:12948856DOI:10.1016/s0006-2952(03)00392-7.

It has previously been shown that the endocannabinoids anandamide and 2-arachidonoylglycerol (2-AG) inhibit the proliferation of C6 glioma cells in a manner that can be prevented by a combination of capsazepine (Caps) and cannabinoid (CB) receptor antagonists. It is not clear whether the effect of 2-AG is due to the compound itself, due to the rearrangement to form 1-arachidonoylglycerol (1-AG) or due to a metabolite. Here, it was found that the effects of 2-AG can be mimicked with 1-AG, both in terms of its potency and sensitivity to antagonism by Caps and CB receptor antagonists. In order to determine whether the effect of Caps could be ascribed to actions upon vanilloid receptors, the effect of a more selective vanilloid receptor antagonist, SB366791 was investigated. This compound inhibited capsaicin-induced Ca(2+) influx into rVR1-HEK293 cells with a pK(B) value of 6.8+/-0.3. The combination of SB366791 and CB receptor antagonists reduced the antiproliferative effect of 1-AG, confirming a vanilloid receptor component in its action. 1-AG, however, showed no direct effect on Ca(2+) influx into rVR1-HEK293 cells indicative of an indirect effect upon vanilloid receptors. Identification of the mechanism involved was hampered by a large inter-experimental variation in the sensitivity of the cells to the antiproliferative effects of 1-AG. A variation was also seen with anandamide, which was not a solubility issue, since its water soluble phosphate ester showed the same variability. In contrast, the sensitivity to methanandamide, which was not sensitive to antagonism by the combination of Caps and CB receptor antagonists, but has similar physicochemical properties to anandamide, did not vary between experiments. This variation greatly reduces the utility of these cells as a model system for the study of the antiproliferative effects of anandamide. Nevertheless, it was possible to conclude that the antiproliferative effects of anandamide were not solely mediated by either its hydrolysis to produce arachidonic acid or its CB receptor-mediated activation of phospholipase A(2) since palmitoyltrifluoromethyl ketone did not prevent the response to anandamide. The same result was seen with the fatty acid amide hydrolase inhibitor palmitoylethylamide. Increasing intracellular arachidonic acid by administration of Arachidonic Acid methyl ester did not affect cell proliferation, and the modest antiproliferative effect of umbelliferyl arachidonate was not prevented by a combination of Caps and CB receptor antagonists.