| Objective: To investigate the effect of galactin-3 antagonist,modified citrus pectin,on heart failure in rabbits after myocardial infarction.To study the mechanism of MCP on ventricular remodeling and myocardial fibrosis in animal models of ischemic heart failure.Methods:1.Animal groups: 30 New Zealand rabbits were randomly divided into Control group,MCP group,perindopril group.2.Process: The left anterior descending coronary arterys of the rabbits were ligatured for model preparation.Rabbits with left ventricular enjection fraction<50% measured with echocardiography 2 weeks after myocardial infarction were enrolled,then they were administered drug of corresponding dose.The Control group was given 0.9% saline 2mL/(kg·d)for 4 weeks.In MCP group,MCP 75mg/mL concentration was dissolved in saline at 2mL/(kg·d)for 4 weeks.Perindopril group was administered with perindopril 0.33mg/mL in saline at 2mL/(kg·d)for 4 weeks.3.Cardiac ultrasound measures before rabbit modelling,2 weeks of modeling,6 weeks of modeling(4 weeks of dosing),left ventricular ejection fraction,left ventricular end diastolic diameter,left ventricular posterior wall thickness.4.The Gal-3 level in serum was measured by ELISA,before modeling,2 weeks after modeling,and 6 weeks of modeling(4 weeks after administration).5.The mRNA expression of Gal-3,Coll I and Coll III in myocardial infarcts and myocardial infarction tissues was detected by Real-Time PCR and the ratio of Coll I/III was calculated.6.Western-Blot detected the expression of Gal-3,Coll I and Coll III proteins in the myocardial infarction tissue and myocardial infarction marginal tissue.7.Myocardial tissue was stained with Masson to observe the pathological changes of myocardium.Results:1.In the Control group,MCP group,and perindopril group,LVEF was less than 50% after 2 weeks of modeling,and compared with that before modeling(P <0.05).After 4 weeks of administration,the cardiac function in MCP group and perindopril group was significantly improved(P <0.01).There was no significant difference between MCP and perindopril in improving left ventricular ejection fraction(P> 0.05).2.After 4 weeks of administration,the serum Gal-3 of MCP group and perindopril group was significantly lower than the Control group(P <0.05).3.After 4 weeks of administration,mRNA expressions of Gal-3,Coll I and Coll III in the MCP group and perindopril group were significantly lower than those in the Control group(P<0.01).MCP and perindopril had no significant difference in the reduction of Gal-3,Coll I and Coll III mRNA in rabbits with ischemic cardiac insufficiency(P>0.05).4.After 4 weeks of administration,the expression of Gal-3,Coll I and Coll III protein in the MCP group and perindopril group was significantly lower than that in the Control group(P<0.05).5.Under the light microscope,a large number of myocardial cell necrosis was observed in the Control group.In group MCP,some myocardial cells showed edema,loose nuclei and collagen deposits around them.In the perindopril group,a small amount of collagen fibers were found in the interstitium of the myocardium,myocardial fibrinolysis,cardiac myocyte edema and hypertrophy in some regions,and a small amount of hyperplasia in the interstitium.Conclusion:1.Gal-3 antagonist-MCP improves cardiac function in rabbits with ischemic heart failure.2.Gal-3 participates in the process of ventricular remodeling and myocardial fibrosis and plays a key role in the cardiac dysfunction.MCP can prevent the expression of gal-3 and improve the process of myocardial fibrosis in the marginal area of myocardial infarction,reconstruction of deterioration,play a role in the treatment of cardiac insufficiency. |
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