Department of Radiation Oncology, Tao Yuan General Hospital, Tao-Yuan, Taiwan, Republic of China.
Inflammation. 2015 Apr;38(2):534-45. doi: 10.1007/s10753-014-9960-8.
Eicosatrienoic acid (Δ11,14,17-20:3; ETrA) is a rare naturally occurring n-3 polyunsaturated fatty acid (PUFA). Using murine RAW264.7 cells, the objectives were to determine how ETrA modulated phospholipid fatty acid compositions and the production of pro-inflammatory mediators. Incubation cells with ETrA dose-dependently increased the proportions of phospholipid ETrA and its metabolites to 33 % of the fatty acid total. Incorporation of ETrA also reduced the proportions of total n-6 PUFA and monounsaturated fatty acids (MUFA) by 30 and 60 %, respectively. ETrA suppressed LPS-stimulated nuclear factor-kappa B (NF-κB)-mediated nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression. However, no such suppressive effect on the production of prostaglandin E2 (PGE2), cytokines, or expression of cyclooxygenase-2 (COX-2) was observed. As compared with ETrA, eicosapentaenoic acid (EPA) exerted a more potent anti-inflammatory effect. In conclusion, although ETrA suppresses significant NO synthesis and iNOS expression, this n-3 PUFA was a less potent anti-inflammatory agent than EPA.
二十碳三烯酸（Δ11,14,17-20:3；ETrA）是一种罕见的天然存在的 n-3 多不饱和脂肪酸（PUFA）。本研究使用鼠源 RAW264.7 细胞，旨在确定 ETrA 如何调节磷脂脂肪酸组成和促炎介质的产生。用 ETrA 孵育细胞可剂量依赖性地增加磷脂 ETrA 及其代谢物的比例，达到脂肪酸总量的 33%。ETrA 的掺入还分别降低了总 n-6 PUFA 和单不饱和脂肪酸（MUFA）的比例 30%和 60%。ETrA 抑制 LPS 刺激的核因子-κB（NF-κB）介导的一氧化氮（NO）产生和诱导型一氧化氮合酶（iNOS）表达。然而，对前列腺素 E2（PGE2）、细胞因子的产生或环氧化酶-2（COX-2）表达没有观察到这种抑制作用。与 ETrA 相比，二十碳五烯酸（EPA）具有更强的抗炎作用。总之，尽管 ETrA 抑制了显著的 NO 合成和 iNOS 表达，但这种 n-3 PUFA 是一种比 EPA 效力较弱的抗炎剂。
