| Background:Myocardial infarction (MI) is a kind of serious threat to human health. Although the effect of interventional therapy for myocardial infarction is very significant, there are still serious complications. Erythropoietin (EPO) not only plays the role in promoting red blood cell proliferation and maturation, but also has some role in organ protection.However, whether EPO can protect the heart of myocardial infarction and the specific protection mechanisms are unclear.Objective:To evaluate the potential protective effect of EPO on cardiac function after myocardial infarction and to explore its possible mechanism.Methods:SD rats were randomly divided into four groups:MI treated with nothing (n=10), continuous treatment group (EA,n=9), intermittent treatment group①(EB,n=9), sham (n=9). After 4 weeks, the rats on the following checks:chocardiography:left ventricular end diastolic dimension(LVEDD); left ventricular end systolic dimension (LVESD); left ventricular ejection fraction (LVEF); fractional shortening (FS);②Hemodynamic:left ventricular peak systolic pressure (LVSP); left ventricular end diastolic pressure (LVEDP), the maximal rising rate of left ventricular pressure (+dP/dt max); the maximal falling rate of left ventricular pressure rise (-dP/dt max);③Histopathological. The rats in SH,MI,EA,EB Groups were sacrificed for HE and Masson.Then the rats in MI,EA,EB Groups were sacrificed for ratsterminal deoxynucleotidyltransferase dUTP nick-end labeling (TUNEL) and reverse transcription-polymerase chain reaction (RT-PCR).All values were compared and statistically analyzed, and P< 0.05 was considered significant.Results:According to echocardiography, hemodynamics and histopathological. results, the ways of acute rat myocardial infarction model were considered to be successful. Echocardiography:MI vsSH. EA,EB, LVEDD (4.75±0.49mm,3.91±0.42mm,4.23±0.42mm,4.33±0.52mm),LVESD (2.31±0.34mm,1.67±0.32 mm,1.77±0.57mm,1.96±0.4mm),LVEF(73.83±6.77%.85.72±5.50%,81.11±5.92%,81.08±7.73%),LVFS(50.21±6.98%,62.26±3.06%,59.96±9.87%, 60.74±7.81%). Hemodynamic:MI vsSH,EA,EB, LVSP (126.96±4.30mmHg, 156.54±4.79 mmHg,148.34±4.49mmHg,145.81±5.18mmHg),LVEDP (23.09±4.24mmHg,18.30±6.68 mmHg,17.49±7.58mmHg,16.69±10.26mmHg),+dP/dtmax(2149.49±73.11mmHg/s,3947.24±92.68 mmHg/s,3243.77±217.37mmHg/s,3126.53±77.55mmHg/s),-dP/dtmax(2459.28±1183.73mmHg/s,3243.77±293.12 mmHg/s,3174.79±233.28mmHg/s,3196.11±351.93mmHg/s).From above, preventive treatment with EPO significantly protected from cardiac dysfunction induced by MI. There was no significant difference between EA Group and EB Group. Histopathological:Normal morphology of myocardial cells disappeared, nuclear shrinkage and vacuolization appear in MI Group.There were inflammatory cell infiltration around and increased myocardial fibrosis in MI, whereas EPO a protective effect in the EA and EB Groups. TUNEL analysis, MI showed apoptotic cells in a patchy distribution, while the apoptotic cells in the EA group and the EB group showed a punctate distribution. There were difference in the proportion of apoptosis cells between MI and EA,EB Groups. RT-PCR assay revealed that compared to the MI Group,the expression level of mRNA was decreased for Caspase-3,Bax in the EA and EB Group. The expression of mRNA were similar for Bcl-2 in MI,EA and EB Group. Also there were no difference between EA and EB Group.Conclusion:Erythropoietin can play protective role in acute myocardial infarction rats through anti-apoptotic mechanism.The molecular mechanism may be associated with the decrease of the expression mRNA level of Bax, Caspase-3. Two different time administration of EPO were similar in the various indicators. |
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