| Objectives1.Observe the influence of midkine (MK) to ventricular remodeling in rats with acute myocardial infarction (AMI);2. Study the influence of midkine (MK) to P-ERK1expression, to further explore the mechanism of MK to ventricular remodeling.MethodsForty-eight adult male Wistar rats were randomly divided into four groups:Control group(n=6), Sham-operated group(n=6), infarct model group (AMI group,n=18), MK treatment group (MK group,n=18).AMI model was established by ligation of left anterior descending coronary artery (LAD);Rats in MK group were injected immediately MK around the LAD after myocardial infarctin; Sham group only hang line, not ligation; Control group will not do anything.Four weeks later, the survived rats were detected haemodynamics, weighed, calculated the whole heart body mass index and prepared specimens.Routine masson’s staining were performed to analyze collagen accumulation.Immunohistochemical staining was carried out in rat heart to quantify neovascularization.Cell apoptosis were tested by TUNEL;Bcl-2、P-ERK1expression in heart was analysed by Western blot.ResultsMK group animals had better cardiac function compared with AMI animals (P<0.01).AMI group animals had higher whole heart body mass index (4.725±0.61) compared with MK animals (3.234±0.189)(P<0.01).Sham group and Control group almost had no collagen formation, and AMI group and MK group have obvious collagen formation.MK animals had higher vascular density (30.165±2.495) in farction area and border-zone area compared with AMI animals (15.206±1.516)(P<0.01). AMI animals had higher cell apoptosis rate than sham-operated group (47.8%±4.5%vs17.4%±1.0%.P<0.01).MK animals had less cell apoptosis rate than AMI animals (27.2%±4.0%vs47.8%±4.5%.P<0.01).MK animals had strongly upregulated the levels of Bcl-2(2.8689±0.4447) compared with AMI animals (1.5727±0.1627)(P<0.01).MK animals had strongly upregulated the levels of phosphorylated extracellular signal-regulated kinase(P-ERK1)(1.1646±0.0092)compared with AMI animals (0.7357±0.0831)(P<0.01).ConclusionsMK prevents ventricular remodeling in rats with acute myocardial infarction;MK can promote angiogenesis in heart of infarction area and infarction border area,inhibit myocardial cell apoptosis,promote the expression of Bcl-2protein;The mechanism may be concerned with upregulation of P-ERK1protein expression. |
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