Anti-inflammatory effect of eicosapentaenoic acid through the modulation of arachidonic acid metabolites in leukocytes.
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概要
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Products derived from arachidonic acid (AA) via both the cyclooxygenase (particularly PGE<SUB>2</SUB>) and lipoxygenase (particularly LTB<SUB>4</SUB>) play a role in inflammation. To clarify the effect of eicosapentaenoic acid (EPA) on inflammation, EPA ethyl ester (80% pure, 240 mg/kg/day) was administered for 4 weeks to the rats. The supplementation of a standard rat diet with EPA caused a significant increase in the formation of LTB<SUB>5</SUB>, which is biologically for less active (at least 30 times) than LTB<SUB>4</SUB>, and a decrease in the synthesis of LTB<SUB>4</SUB> by A 23187 stimulated leukocytes. The EPA rich diet significantly increase the EPA content of leukocytes phospholipids without altering the content of AA, DHA and linoleic acid.<BR>Then, antiinflammatory effect of EPA was assessed using two models of acute inflammation. In the first model EPA fed rat (240 mg/kg/day for 4 weeks) produced significantly lower concentration of PGE<SUB>2</SUB> and TXB<SUB>2</SUB> in inflammatory exudate derived from implantation of carrageenin impregnated sponges. Triene prostaglandin were not detected in the exudate however certain level of LTB<SUB>5</SUB> were present. In the second model, edema induced by injection of carrageenin into rat paws were significantly reduced in animals fed an EPA rich diet. Supplementation of the diet with EPA could, by reducing the synthesis of PGE<SUB>2</SUB> and LTB<SUB>4</SUB> and increasing LTB<SUB>5</SUB> (less active biologically), offer a novel and nontoxic approach to the modulation of an inflammatory response.<BR>Further <I>in vitro</I> experiment disclosed that EPA was better substrate for 5-lipoxygenase than AA but was less favoured substrate for LTA hydrolase. EPA or its oxygenated metabolites, such as LTA<SUB>5</SUB> or LTB<SUB>5</SUB> inhibits LTB<SUB>4</SUB> formation particularly at the level of LTA hydrolase.
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