摘要
以低氧 3h/再给氧 1h期间心肌细胞的生存率、搏动频率、乳酸脱氢酶、丙二醛和超氧化物歧化酶释放为指标 ,观察了蛋白激酶C阻断剂staurosporine和Gi/o蛋白失活剂PTX在低氧预处理和川芎嗪预处理心肌保护中的作用 ,以探讨川芎嗪预处理对心肌缺血再灌注损伤保护作用的机制。结果表明 :分别用staurosporine和PTX处理细胞 10min和 5h后 ,给予低氧预处理和川芎嗪(2 0 μg/ml)预处理 ,心肌细胞在低氧 3h/再给氧 1h后期间 ,其细胞搏动频率、细胞生存率均下降 ;培养液中乳酸脱氢酶和丙二醛释放增多 ,而超氧化物歧化含量下降 ,与单纯低氧 /再给氧组相比均无显著性差异。表明PKC阻断剂和Gi/o蛋白失活剂可取消低氧预处理和川芎嗪预处理对心肌细胞的保护作用 。
In order to understand the intracellular mechanism of preconditioning protection by ligustrazini, we investigated the effects of Gi/o protein and PKC on the spontaneous beating, the survival rate and release of LDH, MDA and SOD in cultured reonatal rat cardiomyocytes treated by HP and ligustrazini during the reoxygenation 1h following hypoxia 3h. The results were as follows: 1) Preconditioning by hypoxia and ligustrazini increased the spontaneous beating and the survival rate, and decreased the release of LDH and MDA with the rise of SOD. 2) Inhibition of Gi/o protein by PTX and PKC by staurosporine abolished the protection by hypoxia preconditioning and ligustrazini with reduction of the beating, survival rate, activity of SOD, and increase of the release of LDH and MDA. The results indicated that activation of signal transduction pathway from Gi/o protein and PKC seem to be involved in the cardioprotection of preconditioning by ligustrazini. [WT5”HZ]
出处
《中药药理与临床》
CAS
CSCD
2001年第3期8-10,共3页
Pharmacology and Clinics of Chinese Materia Medica
