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首页> 外文期刊>Lipids in Health Disease >Dietary supplementation with arachidonic acid increases arachidonic acid content in paw, but does not affect arthritis severity or prostaglandin E2 content in rat adjuvant-induced arthritis model
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Dietary supplementation with arachidonic acid increases arachidonic acid content in paw, but does not affect arthritis severity or prostaglandin E2 content in rat adjuvant-induced arthritis model

机译:日粮中添加花生四烯酸可增加爪中花生四烯酸的含量,但不会影响关节炎的严重程度或大鼠佐剂性关节炎模型中前列腺素E 2 的含量

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Background Arachidonic acid (ARA) is an essential fatty acid and a major constituent of biomembranes. It is converted into various lipid mediators, such as prostaglandin E2 (PGE2), which is involved in the development of rheumatoid arthritis (RA). However, the effects of dietary ARA on RA are unclear. Our objective was to clarify the effects of dietary ARA on an experimental rat arthritis model. Methods Lew rats were fed three contents of ARA diet (0.07%, 0.15% or 0.32% ARA in diet (w/w)), a docosahexaenoic acid (DHA) diet (0.32% DHA), or a control diet. After 4 weeks, arthritis was induced by injection of Freund’s complete adjuvant into the hind footpad. We observed the development of arthritis for another 4 weeks, and evaluated arthritis severity, fatty acid and lipid mediator contents in the paw, and expression of genes related to lipid mediator formation and inflammatory cytokines. Treatment with indomethacin was also evaluated. Results The ARA content of phospholipids in the paw was significantly elevated with dietary ARA in a dose-dependent manner. Dietary ARA as well as DHA did not affect arthritis severity (paw edema, arthritis score, and bone erosion). PGE2 content in the paw was increased by arthritis induction, but was not modified by dietary ARA. Dietary ARA did not affect the contents of other lipid mediators and gene expression of cyclooxygenase (COX)-1, COX-2, lipoxgenases and inflammatory cytokines. Indomethacin suppressed arthritis severity and PGE2 content in the paw. Conclusion These results suggest that dietary ARA increases ARA content in the paw, but has no effect on arthritis severity and PGE2 content of the paw in a rat arthritis model.
机译:背景花生四烯酸(ARA)是必需脂肪酸,也是生物膜的主要成分。它被转化为各种脂质介质,例如前列腺素E2(PGE2),其参与类风湿关节炎(RA)的发展。然而,饮食中ARA对RA的影响尚不清楚。我们的目的是阐明饮食ARA对实验性大鼠关节炎模型的影响。方法喂Lew大鼠3种含量的ARA饮食(饮食中w / w分别为0.07%,0.15%或0.32%ARA),二十二碳六烯酸(DHA)饮食(0.32%DHA)或对照饮食。 4周后,通过将弗氏完全佐剂注入后足垫来诱发关节炎。我们观察了另外四个星期的关节炎的发展,并评估了关节炎的严重程度,爪中脂肪酸和脂质介体的含量以及与脂质介体形成和炎性细胞因子相关的基因的表达。还评估了消炎痛的治疗。结果日粮中ARA的爪中磷脂的ARA含量呈剂量依赖性。膳食ARA和DHA均不影响关节炎的严重程度(爪水肿,关节炎评分和骨侵蚀)。脚掌中PGE2的含量因关节炎诱导而增加,但饮食ARA并未改变。饮食ARA不会影响其他脂质介体的含量以及环氧合酶(COX)-1,COX-2,脂氧合酶和炎性细胞因子的基因表达。消炎痛抑制关节炎的严重程度和爪中PGE2的含量。结论这些结果表明,饮食ARA可增加大鼠关节炎模型中爪子的ARA含量,但对关节炎严重程度和PGE2含量没有影响。

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