Study On Mechanism Of Acute Myocardial Infarction Blood Stagnation Syndrom Permit The Mobilization Of BMSCs Homing And Apr-YTF Intervention

Objective:To find out the relationship between acute myocardial infarction (AMI) Blood Stagnation Syndrom pathogenesis and bone marrow-derived mesenchymal stem cells (BMSCs) mobilization and homing,and find out the effect of active principle region of Yangxing Tongmai Formula(apr-YTF) on mobilization and homing of BMSCs in myocardial infarction AMI Blood Stagnation.Method:1.Literature research:the ancient and modern literature,to understand the cause of AMI Blood Stagnation Syndrom pathogenesis, dialectical characteristics,to understand the mobilization of BMSCs homing,as well as the status of traditional Chinese medicine interventions.2.AMI Blood Stagnation Syndrom permit the mobilization of BMSCs clinical research:collection of AMI Blood Stagnation Syndrom Syndrom,non-effort Stagnation Syndrom e patients and normal subjects of 15 cases,using flow cytometry in peripheral blood CD34+ cell count, blood flow changes in blood flow detected by change indexes,ELISA method of detection of serum vascular endothelial growth factor (VEGF). Comprehensive comparison of the differences among the three groups of indicators to explore the CD34+ cell count and blood rheology and the correlation between VEGF.3.AMI model would be built in a successful effort Stagnation Syndrom e rats were divided into model group,blank control group,recombinant human granulocyte colony stimulating factor (rhG-CSF) group and apr-YTF group,BMSCs were given and the corresponding myocardial injection of drugs,routine HE staining of myocardial infarction pathology,immunohistochemistry of connexin 43 (Cx43),RT-PCR detection of early cardiac developmental genes NKx2.5,to explore the apr-YTF on BMSCs transplantation in rats AMI myocardial infarction Blood Stagnation Syndrom card impact.4.AMI model would be built in a successful effort Stagnation Syndrom e rats were divided into model group,Xiangdan injection group,rhG-CSF group and apr-YTF groups,each to be the appropriate drugs and 5-bromo-deoxyuridine(Brdu) of the intraperitoneal injection,the application PcLab biomedical signal acquisition and processing system, the measurement of cardiac function in rats in vivo;masson's trichrome observing the pathological changes of myocardial tissue,the percentage of ventricular scar size,scar capillary number;flow cytometry in peripheral blood CD34+ cells;immunohistochemical staining of myocardial tissue CD34+ cells,Brdu and cardiac troponin I (cTn I) double staining positive cells,?factor,VEGF,vascular endothelial growth factor receptor (Flk-1),alkali fibroblast growth factor (bFGF) levels.Apr-YTF comprehensive analysis of the mobilization of BMSCs into the blood,orientation and homing into cardiac cells,apr-YTF through the mobilization of BMSCs homing efforts against AMI Stagnation Syndrom e cardiac function in rat myocardial infarction, myocardial morphology changes,Angiogenesis and related cytokine secretion.Result:1.Literature study:Modern literature has greatly widened the AMI Blood Stagnation Syndrom of the etiology and pathogenesis,the relevant organs recognize that there is Blood Stagnation Syndrom AMI basic pathology, the most important is the Qi-deficiency and blood stasis Syndrom e. BMSCs have good prospects for treatment of AMI,which is essential to mobilize homing.2.Clinical Research:AMI effort Stagnation Syndrom e group of hemorheology,blood CD34+ cells,and VEGF with healthy control group,non-effort Stagnation Syndrom e group,the difference was significant. Of non-AMI group effort Stagnation Syndrom e compared with healthy control group,the main indicators differences were also statistically significant. AMI Stagnation Syndrom e group effort Hemorheological and CD34+ cells was negatively correlated, effort Stagnation Syndrom e group and non-permit group Blood Stagnation Syndrom of blood CD34+ cells were positively correlated with VEGF. AMI Blood Stagnation Syndrom cards that although a certain degree of BMSCs to mobilize into the blood,but the effort could significantly impede Stagnation pathology BMSCs mobilized into the blood and its directional homing. BMSCs homing to mobilize the need for good "micro-environment" to improve the Blood Stagnation Syndrom is a way to create this environment.3.Apr-YTF by BMSCs transplantation on rats with myocardial infarction AMI Blood Stagnation Syndrom permit the impact of research shows that: apr-YTF group of animals to restore the best of myocardial infarction, infarct area of inflammatory cells in small infarction area and non-infarct zone limit is not obvious,there are new capillaries;myocardial cells showed Cx43 positive staining granules scattered like change,not just at the end to end connected to the distribution of intercalated disc regions, but also distributed in the side of the membrane on the side of the connection,and even cardiac muscle cells are also short brown-yellow fine particles,apr-YTF group IOD value of the maximum;NKx2.5 each group have a certain level of expression,apr-YTF group expressed the strongest,while the model group,only a very weak expression. Note Yiqihuoxue the apr-YTF can improve AMI Blood Stagnation Syndrom pathogenesis and promote homing of transplanted BMSCs to survive,to improve myocardial infarction pathology,to promote repair.4.By apr-YTF treatment of rats with the mobilization of BMSCs homing efforts AMI study shows the efficacy of Stagnation Syndrom e:apr-YTF can improve the blood and myocardial CD34+ cells,cardiac Brdu and cTn I double staining positive cells,indicating its will to promote BMSCs mobilized into the blood,directed homing and transformed into cardiomyocytes;apr-YTF efforts to improve AMI Stagnation Syndrom e cardiac function in rats with myocardial infarction,reduce ventricular scar area and increased angiogenesis and increased scar-related cytokines (?factor,Flk-1,VEGF,bFGF) secretion,indicating apr-YTF is AMI Blood Stagnation Syndrom by improving the micro-environment to induce the mobilization of BMSCs homing.Conclusion:1.AMI have a basic pathology of the Blood Stagnation.2.AMI Blood Stagnation Syndrom pathology can hinder the mobilization of BMSCs into the blood and its directional homing,BMSCs homing to mobilize the need for good micro-environment,improve Blood Stagnation Syndrom may be ways to create this environment.3.apr-YTF can improve AMI Blood Stagnation Syndrom micro-environment,promoting the mobilization of BMSCs homing to promote the homing of transplanted BMSCs to survive,to improve function of infarcted myocardium and promote repair.