Okita M, Sasagawa T, Suzuki K, Miyamoto A, Wakabayashi H, Watanabe A
Department of Nutritional Science, Faculty of Health and Welfare Science, Okayama Prefectural University, Soja, Japan.
J Nutr Sci Vitaminol (Tokyo). 1998 Dec;44(6):745-56. doi: 10.3177/jnsv.44.745.
The effects of 1% arachidonic acid ethyl ester (AA) administration on the liver prostanoid metabolites and on serum and liver lipids in 3 g/kg ethanol-administered rats fed 10% lard or corn oil were studied. The rats were divided into 6 groups: lard-sucrose (Lard-Suc); lard-ethanol without AA (Lard-Et); lard-ethanol with AA (Lard-EtAA); corn oil-sucrose (Corn-Suc); corn oil-ethanol without AA (Corn-Et); and corn oil-ethanol with AA (Corn-EtAA). Liver triglyceride increased in Corn-EtAA compared with Corn-Et. Arachidonic acid (20: 4n-6) levels in liver phospholipid were significantly decreased in Corn-Et, but elevated in Lard-Et. The levels of 20:4n-6 were significantly increased with AA administration in both ethanol groups. Liver 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in Corn-Suc (24.7 +/- 5.1 pg/mg protein) was markedly higher than in Lard-Suc (4.5 +/- 1.2 pg/mg protein), and the 6-keto-PGF1 alpha lowered significantly with the addition of ethanol (9.3 +/- 0.9 pg/mg protein), but it increased with AA administration (21.6 +/- 4.9 pg/mg protein). In Lard-EtAA, a significant increase in 6-keto-PGF1 alpha was observed compared with Lard-Suc. The liver leukotriene B4 (LTB4) level in Lard-Suc was significantly lower than that of Corn-Suc. In the corn oil group, ethanol feeding was associated with a significant increase in liver LTB4. AA administration to Corn-Et suppressed the elevated LTB4. Serum thiobarbituric acid-reactive substance (TBARS) concentrations in the corn oil group were higher than in the lard group, and these concentrations were not altered by AA administration. From these results, we concluded that the administration of AA in rats treated with ethanol increased 20:4n-6 in liver phospholipid and liver PGI2 levels, irrespective of dietary fat, and may protect against alcoholic liver injury. AA with a diet rich in linoleic acid (18:2n-6), however, may increase fat in the alcoholic liver.
研究了给予1%花生四烯酸乙酯(AA)对喂食10%猪油或玉米油且给予3 g/kg乙醇的大鼠肝脏前列腺素代谢产物以及血清和肝脏脂质的影响。大鼠被分为6组:猪油-蔗糖组(Lard-Suc);猪油-乙醇无AA组(Lard-Et);猪油-乙醇有AA组(Lard-EtAA);玉米油-蔗糖组(Corn-Suc);玉米油-乙醇无AA组(Corn-Et);玉米油-乙醇有AA组(Corn-EtAA)。与Corn-Et组相比,Corn-EtAA组肝脏甘油三酯增加。Corn-Et组肝脏磷脂中花生四烯酸(20:4n-6)水平显著降低,但Lard-Et组升高。在两个乙醇组中,给予AA后20:4n-6水平均显著升高。Corn-Suc组肝脏6-酮-前列腺素F1α(6-keto-PGF1α)(24.7±5.1 pg/mg蛋白)明显高于Lard-Suc组(4.5±1.2 pg/mg蛋白),添加乙醇后6-keto-PGF1α显著降低(9.3±0.9 pg/mg蛋白),但给予AA后升高(21.6±4.9 pg/mg蛋白)。与Lard-Suc组相比,Lard-EtAA组6-keto-PGF1α显著增加。Lard-Suc组肝脏白三烯B4(LTB4)水平显著低于Corn-Suc组。在玉米油组中,喂食乙醇与肝脏LTB4显著增加有关。给予Corn-Et组AA可抑制升高的LTB4。玉米油组血清硫代巴比妥酸反应性物质(TBARS)浓度高于猪油组,且这些浓度不受AA给药的影响。从这些结果中,我们得出结论,在乙醇处理的大鼠中给予AA可增加肝脏磷脂中20:4n-6和肝脏前列环素I2水平,与饮食脂肪无关,且可能预防酒精性肝损伤。然而,AA与富含亚油酸(18:2n-6)的饮食一起,可能会增加酒精性肝脏中的脂肪。