Qiliqiangxin Inhibits Myocardial Injury Induced By Ischemia By Up-regulating Autophagy

Background: Myocardial infarction is a disease caused by coronary atherosclerosis,which leads to coronary artery occlusion,thus causing ischemia and necrosis of surrounding myocardial tissue.At present,there is no radical cure.Autophagy is an important process of intracellular material turnover in eukaryotes.During this process,some damaged proteins or organelles were wrapped by autophagy vesicles with double membrane structure,and then sent to lysosomes or vacuoles for degradation and recycling.Autophagy participated in almost all cell activities.Qiliqiangxin is a traditional Chinese patent medicine for treating heart diseases.Studies have shown that Qiliqiangxin plays an important role in protecting heart remodeling after myocardial ischemia.However,it is unclear whether Qiliqiangxin can regulate autophagy-related proteins to protect myocardial tissue.The purpose of this study is to explore whether Qili can regulate autophagy-related proteins to protect myocardial tissue,so as to provide a new idea for clinical treatment of myocardial infarction。Objective :To investigate whether Qiliqiangxin can regulate autophagy related proteins and inhibit myocardial injury induced by ischemia.Methods: Male wild-type C57BL/6J mice aged 8-12 weeks were selected to establish myocardial infarction model by ligation of anterior descending coronary artery.The mice were randomly divided into sham operation+normal saline group,operation+normal saline group and operation+Qili cardiotonic group(0.25 g/kg d).After operation,the rats were given intragastric administration,and the survival status of mice was recorded every day.After 28 days,the heart function of mice was detected by ultrasound,and then samples were taken to extract tissue protein or RNA,and the related apoptosis index,autophagy level and oxidative stress were detected.In vitro,H9C2 cells were taken as the research object to build a hypoxia model,which was set up as negative group,hypoxia group(treated with 1%H2O2),hypoxia plus Qili cardiotonic group(1x),active oxygen and flow cytometry to detect the apoptosis level.Meanwhile,neonatal rat cardiomyocytes were isolated and transferred into small interfering RNA,and then Qili cardiotonic culture was added to the culture medium for24 h to build the model.Apoptosis and expression of autophagy-related proteins were detected by Western-blotResult :In vivo experiment: the results of ultrasound detection showed that: after myocardial infarction,the cardiac function of mice decreased significantly,and after adding 0.25mg/kg Qiliqiangxin for 28 days,this phenomenon was alleviated.At the same time,the autophagy of myocardial tissue in sham operation group(sham),myocardial infarction(MI)group,myocardial infarction plus Qiliqiangxin group(MI +qlqx)was detected by wetern + blot After adding Qiliqiangxin,this phenomenon was alleviated.In vitro,the results of reactive oxygen species showed that Qiliqiangxin could reduce the content of reactive oxygen species in cells after hypoxia.Wetern-blot was used to detect the related cellular proteins in control group,hypoxia group and hypoxia plus Qiliqiangxin group.It was found that the autophagy level of cells decreased after hypoxia,and this phenomenon was alleviated after Qiliqiangxin was added.At the same time,the expression of apoptotic protein in control group,si-p62 group and si-p62 plus Qiliqiangxin group was detected by wetern-blot.Conclusion:Qiliqiangxin can inhibit myocardial injury induced by ischemia by up regulating autophagy related proteins and then it can protect the myocardium.