Wakabayashi I, Sakamoto K, Hatake K, Tanaka H
Department of Hygiene, Hyogo College of Medicine, Japan.
Eur J Pharmacol. 1994 Apr 1;255(1-3):111-5. doi: 10.1016/0014-2999(94)90088-4.
The effects of aclarubicin on phosphatidylinositol hydrolysis and contractile responses were investigated in isolated rat aorta. In the aclarubicin-pretreated aorta, the basal level of [3H]inositol monophosphate accumulation was significantly lower whereas [3H]phosphoinositide formation was significantly higher than in the saline-pretreated control aorta. Phenylephrine-, 5-hydroxytryptamine- and sodium fluoride-stimulated increases in [3H]inositol monophosphate accumulation were also significantly reduced in the aclarubicin-treated aorta compared to the control. Contractile forces induced by 5-hydroxytryptamine and sodium fluoride were markedly diminished in the aclarubicin-treated aorta. These results suggest that aclarubicin inhibits phosphatidylinositol hydrolysis at a level of phospholipase C activation, which is involved in the reduction of agonist-induced contraction of rat aorta.
研究了阿柔比星对离体大鼠主动脉磷脂酰肌醇水解和收缩反应的影响。在经阿柔比星预处理的主动脉中，[3H]肌醇单磷酸积累的基础水平显著降低，而[3H]磷酸肌醇形成显著高于经生理盐水预处理的对照主动脉。与对照组相比，在经阿柔比星处理的主动脉中，去氧肾上腺素、5-羟色胺和氟化钠刺激引起的[3H]肌醇单磷酸积累增加也显著减少。在经阿柔比星处理的主动脉中，5-羟色胺和氟化钠诱导的收缩力明显减弱。这些结果表明，阿柔比星在磷脂酶C激活水平抑制磷脂酰肌醇水解，这与大鼠主动脉激动剂诱导的收缩减少有关。
