摘要
目的探讨参附注射液(SF)对培养的乳鼠心肌细胞缺氧及缺氧/复氧时凋亡相关基因Fas/FasL蛋白表达的影响。方法按常规培养新生4 d乳鼠心肌细胞,于培养24 h后进行缺氧及缺氧/复氧实验,以免疫组织化学方法检测心肌细胞Fas/FasL蛋白表达的变化。结果缺氧4.5 h及10.5 h后,心肌细胞Fas/FasL蛋白的阳性表达指数(positive expression index,PEI)均显著高于对照。10.5 h组与4.5 h组无明显差异。参附注射液组PEI明显低于缺氧组(P<0.05)。缺氧30 min后再给氧4 h与10 h,心肌细胞Fas/FasL蛋白的PEI显著高于对照,复氧10 h组与4 h组无明显差异,参附注射液组PEI低于无SF组(P<0.05)。结论缺氧及缺氧/复氧时均有凋亡相关基因Fas及其配体FasL蛋白表达的增强,参附注射液可通过下调Fas/FasL蛋白表达,减少凋亡从而减轻缺氧损伤及缺氧/复氧损伤。
Objective To study the effects of SHEN - FU injection on the protein expression of apoptosis - associated Fas/FasL gene in cultured neonatal rat cardiomyocytes with hypoxia and hypoxia- reoxygenation, Methods A cell culture model of neonatal rat cardiomyocytes was used and the treatment was performed with hypoxia and hypoxia- reoxygenation after cardiomyocytes were cultured for 24 hours. The protein expression of Fas/FasL genes were estimated by immunohistochemistry respectively. results Compared with sham- operated group,the positive expression index（PEI）of Fas/FasL proteins in cardiomyocytes increased significantly in the treatment groups after hypoxia for 4.5 and 10.5 hours and there were no differences among hypoxia groups. Compared with hypoxia groups, the PEI of Fas/FasL proteins were lower significantly in groups with SHEN - FU injection treatment（ P 〈 0.05） .After undergoing hypoxia for 30 min and followed by reoxygenation for 4 and 10 hours, the PEI of Fas/FasL proteins in treatment groups were higher significantly than those in sham - operated group and there were no differences among reoxygenation groups. Compared with reoxygenation groups,the PEI of Fas/FasL proteins were lower significantly in the groups with SHEN - FU injection treatment （ P 〈 0.05）. Conclusion In cultured neonatal rat cardiomyocytes, the protein expression of apoptosis- associated Fas/ FasL genes increased.during hypoxia and hypoxia- reoxygenation; The SHEN- FU injection can protect myocardium against hypoxia and hypoxia - reoxygenation injury by downregulating the protein expression of Fas/FasL genes,and then inhibiting myocyte apoptosis.
出处
《中国急救医学》
CAS
CSCD
北大核心
2005年第12期893-895,共3页
Chinese Journal of Critical Care Medicine
基金
中华人民共和国卫生部科研招标课题资助项目(No.200308)
