Comparison of the inhibitory effect of polyunsaturated fatty acids on prostaglandin synthesis. II. Fibroblasts.
In a previous publication we reported that PUFAs of the n-6 and n-3 series caused significant inhibition of synthesis of both PGE2 (28.4-92.8%) and PGF2 alpha (24.4-84.0%) in the oral squamous carcinoma cell line SCC-25. In this report we describe the inhibitory effect of the same acids on PG synthesis in normal human gingival fibroblasts under the same experimental conditions. It was found that a combination of EPA + DCHA (6:4), DCHA and ALA caused significant reduction in synthesis of PGE2 (10.1-87.8%) and PGF2 alpha (14.0-54.6%) at the four dose levels studied. The rank order of potency of acids in reduction of PG synthesis was: EPA + DCHA greater than DCHA greater than EPA greater than ALA greater than LA greater than DGLA greater than GLA. The data suggest that although PUFAs are effective inhibitors of PG synthesis by gingival fibroblasts and SCC-25, the fibroblast is less susceptible to the inhibitory effect of fatty acids.
elAttar
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Laboratory of Hormone Research, University of Missouri School of Dentistry, Kansas City 64108.
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Platt
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D000328:Adult; D015237:Dinoprost / Q000096:biosynthesis*; D015232:Dinoprostone / Q000096:biosynthesis*; D004281:Docosahexaenoic Acids / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D015118:Eicosapentaenoic Acid / Q000494:pharmacology; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology*; D005260:Female; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism*; D005881:Gingiva / Q000166:cytology; D006801:Humans; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000494:pharmacology; D008042:Linolenic Acids / Q000494:pharmacology; D017962:alpha-Linolenic Acid
D005231:Fatty Acids, Unsaturated; D008041:Linoleic Acids; D008042:Linolenic Acids; D017962:alpha-Linolenic Acid; D004281:Docosahexaenoic Acids; D019787:Linoleic Acid; D015118:Eicosapentaenoic Acid; D015237:Dinoprost; D015232:Dinoprostone