摘要
目的探讨银杏内酯B对体外培养乳鼠心肌细胞氧化损伤的保护作用及其机制。方法利用低浓度过氧化氢诱导原代培养乳鼠心肌细胞氧化损伤为模型 ,通过电镜观察细胞超微结构,以及培养介质中LDH活力 ,MDA含量 ,心肌细胞内Na+ -K+ -ATPase,GSH -PX活力的改变 ,来评价银杏内酯B对心肌细胞的保护作用 ,并探讨其机制。结果过氧化氢对心肌细胞有显著的损伤作用。银杏内酯B可使培养介质中的LDH和MDA水平显著下降 ,细胞内Na+ -K+ -ATPase,GSH -PX活力显著提高 ,同时细胞超微结构得到改善。结论银杏内酯B对过氧化氢致心肌细胞损伤有保护作用 。
Objective To determine whether the administration of ginkgolide B is able to protect cardiomyˉocytes against oxidative stress.Methods An experimental model of oxidative injury was established by using culˉtured neonatal rat cardiomyocytes.Myocyte damages were estimated by lactate dehydrogenase(LDH)release and ulˉtrastructural morphological alteration.Malondialdehyde(MDA)content was measured as an index of lipid perioxidaˉtion.The activity of Na + -K + -adenosine triphosphatase(Na + -K + -ATPase)and glutathione peroxidase(GSH-PX)were also assayed.Results GinkgolideB treatment significantly decreased LDH leakage and MDA production and restored activities of Na + -K + -ATPase and GSH-PX to control level.Conclusions Pretreatment with ginkgolide B protects cardiomyocytes from induced injury and the beneficial effect may be related to its antioxidant properties and thus protect Na + -K + -ATPase from oxidative stress.
出处
《中国微循环》
2004年第4期213-215,共3页
Journal of Chinese Microcirculation
关键词
银杏内酯B
心肌细胞
氧化损伤
钠钾泵
Ginkgolide B
Cardiomyocytes
Oxidative stress
Na + -K + -ATPase