| ObjectiveThis study intended to explore the protective effect of exogenous apelin on heart aftermyocardial infarction in ratand analyze the mechanism of this protective effect which is related to whether apelin mediated mobilization of cardiac stem cells in vivo.Methods1. Animal models of male SD rats after acute myocardial infarction was constructed by left anterior descending coronary artery ligation. Then the experimental group was completed respectively according to the following way: the rats of sham-operated group underwent thoracic surgery without both coronary artery ligation and drug injection; the rest rats ofboth control and experimental groups underwent intramyocardial injection with saline solution20μl and apelin-130.2μg/20μl within5min after coronary artery ligation, respectively.2. Color doppler sonography detected ejection fraction, left ventricular end-diastolic diameter, left ventricular end-systolic diameter and fractional shortening two weeks after operation so as to evaluate the changes of cardiac function.3.Detected myocardial infarct area by using TTC staining method.4. Immunohistochemical staining method was used to detect the positive expression of C-kit, Scal and Flk1in myocardial tissue.5. Western blotting and Real Time-PCR were further used to quantitatively examine the expression levels of C-kit,Scal and Flk1protein and mRNA in myocardial tissue.Results1.20male SD rats were randomly divided into3groups: sham-operated group (n=6), control group (AMI+saline solution, n=12), experimental group (AMI+apelin-13,n=12). Four rats died in the control group and five in the experimental group.2. The results of echocardiography and myocardial infarct size measurement showedthat cardiac function of rats was improved more significantly in experimental group than incontrol group (EF:68.43%±2.06%in experimental group and46.40%±15.18%in controlgroup; FS:33.70%±1.55%in experimental group and20.73%±8.14%in control group; infa rction myocardial area percentage:16.10%±3.08%in experimental group and33.83%±5.64%in control group; P<0.05).3. Immunohistochemical staining of C-kit, Sca1and Flk1was negative in sham-operated group and positive or strong positive both in experimental group and control group.4. Western blotting and Real Time-PCR showed that the protein and mRNA expression of C-kit, Sca1and Flk1were significantly higher in experimental group than in control group (protein level: C-kit0.48±0.17vs1.05±0.08, Sca10.39±0.08vs0.70±0.08, Flk10.40±0.26vs0.88±0.10,P<0.05; mRNA level: C-kit2.89±1.89vs18.77±14.19, Sca14.32±2.44vs29.39±11.90, Flk12.14±0.95vs4.59±0.92, P<0.05),and there was no obvious expression of C-kit, Sca1or Flk1protein in sham-operated group.Conclusion1.The input of exogenous apelin-13can alleviate myocardial injury, enhancemyocardial contractility, and improve heart function in acute ischemic myocardial injury.2. Exogenous apelin-13can play a protective role on myocardial injury through the mobilization and proliferation of cardiac stem cells in vivo. |
PDF Full Text Request