摘要
目的观察不同配伍比例的附子人参对缺糖缺氧/复糖复氧损伤大鼠心肌细胞的保护作用。方法将原代培养6 d的心肌细胞分为正常对照组、模型组、不同配伍比例的附参组、空白血清组。建立原代大鼠心肌细胞缺糖缺氧/复糖复氧损伤模型,观察不同配伍比例的附子人参血清对损伤心肌细胞自发搏动、细胞活力的作用,并测定心肌细胞中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量以及心肌组织上清液中一氧化氮(NO)分泌量和乳酸脱氢酶(LDH)释放率。结果与空白血清组比较,各附参配伍组心肌细胞自发搏动频率、细胞活力显著升高(P<0.05),心肌细胞SOD活性显著升高(P<0.05),MDA含量、NO分泌量和LDH释放率均显著降低(P<0.05),而且附参(2∶1)组对心肌细胞的自发搏动频率、细胞活力、SOD、MDA和LDH作用均不同程度地优于其余各配伍组。结论各附参配伍组对缺糖缺氧/复糖复氧损伤大鼠心肌细胞具有保护作用,其中以附参(2∶1)组作用效果最为显著。
Objective To evaluate the protective effect of Radix Aconiti Lateralis Praeparata（Fuzi） and Radix Ginseng（Renshen） at different compatibility proportions on oxygen/glucose deprivation and reintroduction（OGD/R） injury in neonatal rat cardiomyocytes.Methods The neonatal rat cardiac muscle cells after primary culture for 6 days were randomly divided into normal control group,model group,Fuzi-Renshen groups,and blank serum group.We established the injury model of primary neonatal rat cardiac muscle cells by OGD/R,and observed the effect of drug serum of Fuzi-Renshen at different compatibility proportions on spontaneous impulse frequency and viability of the injured neonatal rat cardiomyocytes,and on superoxide dismutase（SOD）,malondialdehyde（MDA）,nitric oxide（NO） and lactate dehydrogenase（LDH） contents in the injured cardiomyocytes.Results Compared with the blank serum group,spontaneous impulse frequency,cell viability,SOD activities were increased obviously,and MDA content,NO content and the release rate of LDH were decreased obviously（P〈0.05） in Fuzi-Renshen groups（P〈0.05）.Fuzi-Renshen at the compatibility proportion of 2 ∶ 1 had better effect than other compatibility proportions.Conclusion Fuzi-Renshen at different compatibility proportions shows significant protective effect on neonatal rat cardiomyocytes with OGD/R injury,and compatibility proportion of 2∶ 1 has the best effect.
出处
《中药新药与临床药理》
CAS
CSCD
北大核心
2015年第2期148-152,共5页
Traditional Chinese Drug Research and Clinical Pharmacology
基金
国家自然科学基金资助项目(81173597)
关键词
附子
人参
配伍
缺糖缺氧/复糖复氧
心肌细胞
Radix Aconiti Lateralis Praeparata
Radix Ginseng
Compatibility
Oxygen/glucose deprivation and reintroduction
Cardiac muscle cells
