摘要
目的观察强心方对心力衰竭小鼠心功能及梗死区心肌组织细胞纤维化和心室重构(ventricular remodeling,VR)的影响。方法将48只雄性C57小鼠腹腔注射阿霉素制作心力衰竭模型,于造模成功后分别给予强心方低剂量及高剂量灌胃,连续灌胃1个月后通过超声心动图检测各组小鼠心功能水平,随后取材。ELISA检测小鼠血清BNP水平,Masson三色染色分别观察梗死区胶原纤维沉积,RT-qPCR检测小鼠心脏组织Anp、β-MHC基因表达水平。结果心力衰竭发生后,相较于模型组,强心方治疗各组超声心动图检测表明其心功能水平提升,ELISA检测发现心力衰竭指标BNP水平降低,Anp、β-MHC基因表达提示抑制心肌肥大,Masson三色染色分别观察梗死区胶原纤维沉积减少。结论强心方可以一定程度上改善慢性心力衰竭小鼠心功能水平,其可能通过小鼠减轻心肌肥厚、纤维化等多途径延缓心室重构进程。
Objective To observe the effect of Qiangxinfang on cardiac function,myocardial tissue fibrosis and ventricular remodeling in infarcted mice with heart failure.Methods In this study,48male C57mice were injected intraperitoneally with doxorubicin to make a heart failure model.Then they were given low-dose or high-dose of Qiangxinfang by intragastric administration.The levels of rat heart function were obtained.The levels of BNP in the blood circulation were detected by ELISA,the collagen fiber deposition in the infarcted area was observed by Masson′s trichrome staining,and the expression levels of Anp andβ-MHC genes in the mouse heart tissue were detected by RT-qPCR.Results After the occurrence of heart failure,compared with the model group,each group treated with Qiangxinfang showed improved cardiac function by echocardiography,and decreased levels of BNP heart failure indicators by ELISA detection.We also observed decreased deposition of collagen fibers in the infarcted area by Anp、β-MHC genes and Masson′s trichrome staining.Conclusion Qiangxinfang can improve the cardiac function of chronic heart failure mice to a certain extent,and it may delay the process of ventricular remodeling by reducing myocardial hypertrophy and fibrosis in mice.
作者
曹巍巍
刘晨萍
袁晨越
薛永鹏
CAO Weiwei;LIU Chenping;YUAN Chenyue(Shanghai Municipal Hospital of Traditional Chinese Medicine,Shanghai University of TCM,Shanghai 200071,China)
出处
《医学研究杂志》
2023年第6期112-116,共5页
Journal of Medical Research
基金
上海市卫生健康委员会卫生行业临床研究专项面上项目(201940236)
上海中医药大学预算内项目(2021LK066)
上海中医药大学附属市中医医院未来计划项目(WL-HBQN-2021002K)。
关键词
慢性心力衰竭
心功能水平
心室重构
心肌纤维化
小鼠
Chronic heart failure
Cardiac function level
Ventricular remodeling
Myocardial fibrosis
Mice
