摘要
该研究首先建立过氧化氢(H2O2)诱导大鼠胚胎心肌细胞株(H9c2)氧化损伤模型,并筛选出益气活血方肠吸收液体外心肌保护作用的浓度范围,优选出4个剂量进行实验;通过考察益气活血方肠吸收液对H9c2的保护作用,从而为临床防治与氧化应激损伤相关心脏疾病提供参考;并通过对H9c2心肌细胞活力、细胞形态、超氧化物歧化酶(SOD)、丙二醛(MDA)等指标进行考察,对益气活血方肠吸收液作用机制进行初步评价探讨。结果显示,益气活血方肠吸收液对H2O2诱导H9c2心肌细胞损伤具有较好的保护作用,且呈现出一定的浓度依赖性,可提高SOD的活性,减少MDA的释放,从而降低异常细胞的形成,增强心肌细胞抗氧化能力,提高细胞活力,具有一定的保护作用。
This research firstly establishes the oxidative damage model of H9c2 induced by H2O2 and screens the concentration range of intestines absorption liquid of Qi benefiting and blood circulation activating formula which possess external myocardium protection function. Then,the thesis chooses 4 dosages to conduct experiments: examining the protection function of intestines absorption liquid of Qi benefiting and blood circulation activating formula on H9c2 to provide reference for clinical prevention and curing of relative heart diseases of oxidative stress injury; as well as examining the H9c2 cardiac muscle cell vigour,cellular morphology,SOD,MDA and other indexes to primarily evaluate and discuss the functional mechanism of intestines absorption liquid of Qi benefiting and blood circulation activating formula. The results show that the intestines absorption liquid of Qi benefiting and blood circulation activating formula has relatively better protection function toward the H9c2 cardiac muscle cell damage induced by H2O2 and presents concentration dependency to some extent. The intestines absorption liquid of Qi benefiting and blood circulation activating formula can increase SOD vigour,and decrease MDA emission,thus decreasing the formation of abnormal cell and strengthening the oxidation resistance of cardiac muscle cell. The intestines absorption liquid of Qi benefiting and blood circulation activating formula has protection function to some extent.
出处
《中国中药杂志》
CAS
CSCD
北大核心
2016年第20期3821-3827,共7页
China Journal of Chinese Materia Medica
基金
国家自然科学基金项目(81273625)
国家"重大新药创制"科技重大专项(2014ZX09201021-009)
国家重点基础研究发展计划(973)项目(2015CB554406)
关键词
益气活血方
心肌细胞
氧化应激
MDA
SOD
supplementing Qi and activating blood circulation
myocardial cells
oxidative stress
MDA
SOD