Morisaki N, Shinomiya M, Matsuoka N, Saito Y, Kumagai A
Tohoku J Exp Med. 1983 Dec;141(4):397-405. doi: 10.1620/tjem.141.397.
Highly purified cis-5,8,11,14,17-20:5 (n-3) or cis-4,7,10,13,16,19-22:6 (n-3) was administered to rats for 2 weeks, and serum lipoprotein lipid levels, platelet aggregation, and lipid metabolism in the aorta in vivo were investigated. 20:5 (n-3) decreased the level of low density lipoprotein phospholipid. 22:6 (n-3) increased the level of high density lipoprotein cholesterol and decreased those of low density lipoprotein triglyceride and phospholipid. Both 20:5 (n-3) and 22:6 (n-3) markedly inhibited platelet aggregation. 20:5 (n-3) decreased the acid and neutral cholesterol esterase activities, but did not affect either acyl-CoA synthetase or acyl-CoA: cholesterol acyltransferase activity. 22:6 (n-3) had no effect on any of these enzyme activities. From these results, the roles of 20:5 (n-3) and 22:6 (n-3) in the formation of atheromatous lesions and the mechanism of the decrease in cholesterol esterase activity by 20:5 (n-3) were discussed.
将高度纯化的顺式-5,8,11,14,17-二十碳五烯酸（n-3）或顺式-4,7,10,13,16,19-二十二碳六烯酸（n-3）给予大鼠2周，然后研究体内血清脂蛋白脂质水平、血小板聚集以及主动脉中的脂质代谢。二十碳五烯酸（n-3）降低了低密度脂蛋白磷脂水平。二十二碳六烯酸（n-3）提高了高密度脂蛋白胆固醇水平，并降低了低密度脂蛋白甘油三酯和磷脂水平。二十碳五烯酸（n-3）和二十二碳六烯酸（n-3）均显著抑制血小板聚集。二十碳五烯酸（n-3）降低了酸性和中性胆固醇酯酶活性，但对酰基辅酶A合成酶或酰基辅酶A：胆固醇酰基转移酶活性均无影响。二十二碳六烯酸（n-3）对这些酶活性均无影响。根据这些结果，讨论了二十碳五烯酸（n-3）和二十二碳六烯酸（n-3）在动脉粥样硬化病变形成中的作用以及二十碳五烯酸（n-3）降低胆固醇酯酶活性的机制。
