摘要
目的研究蛇床子素对阿霉素引起的心脏毒性的影响,并探讨其作用机制。方法用给SD大鼠ip阿霉素(ADR)的方法复制ADR心脏毒性模型。采用颈总动脉插管的方法,用十六导生理记录仪测定大鼠的血流动力学各项指标,酶促反应定磷比色法测定心肌肌浆网(SR)Ca2+-ATP酶的活性。结果蛇床子素对ADR引起的心脏毒性大鼠的血流动力学有明显改善作用,能显著升高心肌SRCa2+-ATP酶的活性。结论蛇床子素对ADR引起的心脏毒性有保护作用,其作用机制可能与激活SR膜Ca2+-ATP酶、促进Ca2+储备、降低胞浆中Ca2+浓度、阻止Ca2+超载有关。
Objective To observe the effect of osthol （Ost） against chronic eardiotoxicity induced by adriamycin （ADR）. Methods The cardiotoxieity model was established by ip ADR in SD rats, on which common carotid artery cannulation were later operated. Hemodynamical changes were detected by sixteen channel datare corder system, and the activity of myocardial SR Ca^2＋-ATPase were determined by enzymatic reaction colorimetric determination phosphorus. Results Ost improved the haemodynamical parameters of rats with ADR- induced cardiotoxicity, and increased the activity of myocardial SR Ca^2＋-ATPase. Conclusion Osthol has a protective effect on ADR-indueed cardiotoxicity. The mechanism may be related to its function of activating SR Ca^2＋-ATPase, promoting Ca^2＋ storage, decreasing Ca^2＋ concentration, and inhibiting Ca^2＋ overload.
出处
《现代药物与临床》
CAS
2009年第6期358-360,共3页
Drugs & Clinic
