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伤肌宁胶囊对抗阿霉素所致心肌细胞凋亡及其相关基因BCL-2 BAX蛋白表达影响
引用本文:张景红,樊秦.伤肌宁胶囊对抗阿霉素所致心肌细胞凋亡及其相关基因BCL-2 BAX蛋白表达影响[J].中医药学刊,2010(6):1252-1255.
作者姓名:张景红  樊秦
作者单位:[1]华侨大学分子药物研究所,福建泉州362021 [2]甘肃中医学院中心试验室,甘肃兰州730000 [3]兰州大学生命学院,甘肃兰州730000
基金项目:福建省重点资助项目(2008Y0055); 泉州市科技资助项目(2008Z76); 华侨大学高层次人才科研启动项目(08BS105) 致谢:在本文的实验过程中得到甘肃中医学院动物试验中心的张延英和蔺心遥老师的指导,特此感谢.
摘    要:目的:观察含伤肌宁胶囊的大鼠血清(SJNXQ),对阿霉素(ADR)所致心肌细胞凋亡的抑制作用及其对相关基因BCL-2、BAX蛋白表达的影响。方法:血清药理学方法制备"伤肌宁胶囊"含药血清(SJNJN);SD乳鼠心肌细胞做原代培养,复制ADR损伤心肌细胞模型,并运用流式细胞仪检测细胞凋亡及其相关BAX和BCL-2蛋白的表达。结果:心肌细胞给予ADR后,心肌细胞凋亡指数明显升高,BAX蛋白表达升高;BCL-2蛋白表达明显降低。含伤肌宁胶囊的血清,能显著抑制心肌细胞凋亡,降低BAX蛋白表达,提高BCL-2蛋白的表达水平,其效应呈剂量依赖关系。结论:伤肌宁胶囊具有拮抗阿霉素所致心肌细胞凋亡作用,其机制可能与SJNXQ提高BCL-2/BAX比值特性有关。

关 键 词:伤肌宁胶囊含药血清  阿霉素  心肌细胞凋亡  BCL-2和BAX蛋白

Inhibitory Effects of the Medicated Serum of ShangJiNing Capsules on Cultured Neonatal Rat Cardiomyocyte Apoptosis and the Expression of BCL-2,BAX Protein Induced by Adriamycin(ADR)
ZHANG Jing-hong,FAN Qin.Inhibitory Effects of the Medicated Serum of ShangJiNing Capsules on Cultured Neonatal Rat Cardiomyocyte Apoptosis and the Expression of BCL-2,BAX Protein Induced by Adriamycin(ADR)[J].Study Journal of Traditional Chinese Medicine,2010(6):1252-1255.
Authors:ZHANG Jing-hong  FAN Qin
Institution:1.Insititute Molecular Medicine,Huaqiao University,Quanzhou 362021,Fujian,China;2.Medical Trial Center ,Gansu College of Traditional Chinese Medicine,Lanzhou 730000,Gansu,China;3.Life science,Lanzhou University,Lanzhou 730000,Gansu,China)
Abstract:Objective:To investigate the inhibitory effect of the medicated serum of ShangJiNing capsules (SJNXQ) on cultured neonatal rat cardiomyocyte apoptosis and the expression of BCL-2,BAX protein induced by adriamycin(ADR). Methods:The serums were prepared from ShangJiNing capsules pellet-fed wistar rats administered; and primary culture neonatal SD rat cardiac myocyte and ADR injury model were established. Apoptotic cardiomyocytes and the expression of BAX and BCL-2 proteins were determined using the using flow cytometry. Results:Compared with control group,ADR group had significantly higher proportion of apoptotic cardiomyocytes. The expression of BAX protein in ADR group was significantly higher than that in control group,however the expression of BCL-2 protein was significantly lower than that in control group. SJNXQ significantly inhibited the cardiomyoctes from apoptosis induced by ADR,and the elevated the expression of BCL-2 protein,which was closed to that of control group,and also decreased the levels of BAX protein as well,revealing the relationship to dose-dependence. Conclusion:Myocardial apoptosis is an important mechanism of adriamycin-induced cardiomyopathy. SJN can inhibit cardiomyocyte apoptosis,partly because it might increase the ratio of BCL-2/BAX.
Keywords:medicated serum of ShangJiNing capsules  adriamycin  cardiomocyte apoptosis  BCL-2  BAX Protein
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