摘要
目的观察山莨菪碱(Ani)对阿霉素(ADR)所致培养的心肌细胞毒性作用的影响,并初步探讨了其作用机制.方法采用原代培养的SD大白鼠乳鼠心肌细胞,以1.84 μmol·L-1阿霉素造成急性心肌细胞中毒模型,Ani作用浓度为40.7～407 μmol·L-1.测定心肌细胞乳酸脱氢酶(LDH)释放量、心肌细胞搏动频率及线粒体琥珀酸脱氢酶(SDH)的活力.结果阿霉素引起心肌细胞LDH漏出明显增加,SDH活力降低,心肌细胞搏动频率异常.应用不同浓度Ani,可不同程度地减轻阿霉素所致心肌细胞LDH漏出量、SDH活力降低和搏动频率的降低.结论山莨菪碱对阿霉素中毒心肌细胞具有保护作用,其机制可能与保护心肌细胞线粒体有关.
Objective To determine the protective role of Anisodamine against adriamycin-induced eardiotoxieity in cultured myocardial cells. Methods Primary cultured myocardial cells were treated with Adriamyein （18.4μmol·L^-1） and Adriamyein ＋ Anisodamine （40.7-407μmol·L^-1 ） . Lactate dehydrogenase （LDH） activity, the activity of sueeino-dehydrogenase （SDH） in the mitochondria and the beating rate of myocardial cells were askayed. Results LDH activity was significantly in- creased in adriamyein group compared with that in the control group, and the beating rate was abnormal and the activity of SDH was reduced. Meanwhile, in adriamyein ＋ Anisodamine of different concentrations groups, on different degrees Anisodamine might reduce the leakage of LDH from myocardial cells, and inhibit the abatement of SDH activity. And the amendment of cells beating was observed. Conclusions Anisodamine has protective effects on adriamyein-induced eardiotoxieity in cultured myocardial cells, and its mechanism may be related to protect the mitochondria.
出处
《锦州医学院学报》
2005年第6期19-21,共3页
Journal of Jinzhou Medical College
关键词
阿霉素
山莨菪碱
培养心肌细胞
心肌毒性
adriamycin
anisodamine
cultured myocardial cells
cardiotoxicity
