Chaet M S, Garcia V F, Arya G, Ziegler M M
Department of Surgery, Children's Hospital Research Foundation, University of Cincinnati, Ohio 45229.
J Surg Res. 1994 Jul;57(1):65-8. doi: 10.1006/jsre.1994.1111.
Nitric oxide (NO) is recognized as an important mediator of hemodynamic regulation and multisystem organ failure (MOF). Although polyunsaturated fatty acids (PUFA) are known to modify the elaboration of some humoral mediators in MOF, their effect upon NO production has not been evaluated. This study was designed to examine the effect of omega-3 (omega 3) and omega-6 (omega 6) PUFA on macrophage production of NO, TNF, PGE2, and PGI2. Rats were fed diets of 18% by calorie safflower oil (omega 6) or fish oil (omega 3) for 12 days. Bronchoalveolar macrophages (BAM) were divided into group A (medium only), group B (0.5 microgram/ml PGE2 or PGI2 + medium) or group C (10 microM indomethacin+medium). Cells were stimulated with 100 U/ml interferon-gamma and 10 micrograms/ml Escherichia coli-LPS. In group A, BAM from animals fed omega 3 produced significantly more NO (3.64 vs 1.92 microM, P < 0.05) and TNF (8.52 vs 1.75 micrograms/ml, P < 0.05) than BAM from omega 6-fed animals. The addition of exogenous PGE2 or PGI2 (group B) ablated the difference in NO and TNF observed in group A. Indomethacin also (group C) ablated the difference in NO and TNF production seen in omega 3- and omega 6-fed animals noted in group A. These data demonstrate that PUFA influence BAM production of NO and TNF. Changes in the omega 6-derived prostanoids may account for the differences in TNF production, but these data suggest that PGE2 and PGI2 are not responsible for the observed differences in NO production.(ABSTRACT TRUNCATED AT 250 WORDS)
一氧化氮(NO)被认为是血流动力学调节和多系统器官衰竭(MOF)的重要介质。尽管已知多不饱和脂肪酸(PUFA)可改变MOF中某些体液介质的产生,但它们对NO生成的影响尚未得到评估。本研究旨在检测ω-3(omega 3)和ω-6(omega 6)PUFA对巨噬细胞产生NO、肿瘤坏死因子(TNF)、前列腺素E2(PGE2)和前列环素(PGI2)的影响。给大鼠喂食热量为18%的红花油(ω-6)或鱼油(ω-3)饮食12天。支气管肺泡巨噬细胞(BAM)分为A组(仅培养基)、B组(0.5微克/毫升PGE2或PGI2+培养基)或C组(10微摩尔/升吲哚美辛+培养基)。细胞用100单位/毫升干扰素-γ和10微克/毫升大肠杆菌脂多糖刺激。在A组中,喂食ω-3的动物的BAM产生的NO(3.64对1.92微摩尔,P<0.05)和TNF(8.52对1.75微克/毫升,P<0.05)明显多于喂食ω-6的动物的BAM。添加外源性PGE2或PGI2(B组)消除了A组中观察到的NO和TNF的差异。吲哚美辛(C组)也消除了A组中喂食ω-3和ω-6的动物在NO和TNF产生上的差异。这些数据表明PUFA影响BAM产生NO和TNF。源自ω-6的前列腺素的变化可能是TNF产生差异的原因,但这些数据表明PGE2和PGI2不是观察到的NO产生差异的原因。(摘要截短至250字)