Nakao J, Chang W C, Murota S, Orimo H
Atherosclerosis. 1981 Jul;39(4):439-45. doi: 10.1016/0021-9150(81)90001-0.
The effect of triiodothyronine (T3) on prostacyclin production in rat aortic smooth muscle cells was investigated by using an intact cell assay system. T3 at its physiological concentrations has no significant effect on smooth muscle cell proliferation, but it does significantly stimulate prostacyclin production by the cells. Maximum stimulation of prostacyclin production is obtained when cells are treated with T3 for 4 consecutive days. The dose--response curve shows a linear relationship between the stimulation of prostacyclin production and T3 concentrations in the range 0.007--10 microgram/dl. The maximal prostacyclin production by T3-treated cells (at a concentration of 10 microgram/dl), is 270% compared with control cells. T3 treatment shows no significant effect on phospholipase (and/or lipase) activities. Our results suggest that thyroid hormone might play an important physiological role in the protection of arteries from atherosclerotic changes by stimulating prostacyclin production in arterial smooth muscle cells.
利用完整细胞分析系统研究了三碘甲状腺原氨酸(T3)对大鼠主动脉平滑肌细胞前列环素生成的影响。生理浓度的T3对平滑肌细胞增殖无显著影响,但能显著刺激这些细胞生成前列环素。当细胞连续4天用T3处理时,可获得前列环素生成的最大刺激作用。剂量-反应曲线表明,在0.007 - 10微克/分升范围内,前列环素生成的刺激作用与T3浓度之间呈线性关系。与对照细胞相比,经T3处理的细胞(浓度为10微克/分升)产生的最大前列环素量为270%。T3处理对磷脂酶(和/或脂肪酶)活性无显著影响。我们的结果表明,甲状腺激素可能通过刺激动脉平滑肌细胞生成前列环素,在保护动脉免受动脉粥样硬化改变方面发挥重要的生理作用。