摘要
目的 :探讨黄芩苷对缺氧缺糖性心肌细胞的影响。方法 :取SD乳鼠的心脏 ,经消化 ,分离及纯化制成心肌细胞悬液并接种至 2 4孔培养板中 ,通过缺氧缺糖 ,建立心肌细胞“缺血性”损伤的实验病理模型 ,在此基础上观察黄芩苷对缺氧缺糖心肌细胞形态及细胞内SOD、MDA水平及NO分泌的影响。结果 :0 1～ 10 μg/ml的黄芩苷可显著提高缺氧性心肌细胞中SOD活性 ,10 μg/ml的黄芩苷显著抑制MDA的生成 ,1μg/ml黄芩苷显著增加NO分泌 ,10 μg/ml黄芩苷又抑制NO分泌。 结论 :黄芩苷对缺氧缺糖性心肌细胞损伤具有一定的保护作用。
AIM:To observe the effect of baicalin on hypoxia injury in neonatal rat cardiomyocytes. METHOD:Isolation of cardiomyocytes from Sprague Dawley rats aging 2～3 d hearts was performed. The cell density was adjusted to 1×10 9 cell·L -1 ,and 1 ml of the suspension was pipeted into each well of 24 well culture plates. The effect of baicalin on superoxde dismutase(SOD), malondialdehyde(MDA) and Nitric oxide(NO) was investigated in vitro in neonatal rat cardiomyocytes during hypoxia injury. RESULT:0 1～10 μg/ml doses of Baicalin increased remarkable SOD activity during hypoxia injury. 10 μg/ml Baicalin could significantly inhabite MDA production; 1 μg/ml baicalin increased remarkably the level of nitrio oxide ,10 μg/ml baicalin inhabite the level of nitrio oxide. CONCLUSION:The results indicate that baicalin has a protective effect on hypoxia injury in neonatal rat cardiomyocytes.
出处
《中国药科大学学报》
CAS
CSCD
北大核心
2003年第1期55-57,共3页
Journal of China Pharmaceutical University
基金
铁道部科技基金 (编号J98Z0 0 2 )
江苏省科委社会发展研究资助项目 (编号BS960 36)~~
