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Expression Of Galectin-3 In Rabbits With Ischemic Cardiac Dysfunction And Its Role In Ventricular Remodeling

Posted on:2019-02-20Degree:MasterType:Thesis
Country:ChinaCandidate:Y H ZhangFull Text:PDF
GTID:2394330566979281Subject:Internal medicine
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Objective:By detecting the expression of galectin-3(Gal-3)in myocardial tissue and serum changes of rabbits with ischemic cardiac dysfunction and analyzing the relationship between Gal-3 and myocardial fibrosis,we explored the role of Gal-3 in ventricular remodeling.Methods:1 Twenty rabbits were randomly assigned to sham group(n=10)or cardiac dysfunction group(n=10)using random number table method?2 Ischemic cardiac dysfunction model was made by ligation of the anterior descending coronary artery.Rabbits with left ventricular enjection fraction(LVEF)<50% measured with echocardiography 2 weeks after operation indicated that model was made successfully.Sham group rabbits were only subjected to thoracotomy without coronary artery ligation.Animals were sacrificed at 6 weeks after operation.3 Cardiac function was measured by echocardiography before operation,2 weeks after operation and 6 weeks after operation respectively.LVEF and left ventricular end diastolic diameter(LVEDD)were recorded.4 Real-time PCR and Western-Blot methods were used to detect the mRNA and protein expression of Gal-3,type I collagen and type III collagen in the myocardial infarction tissue of rabbits with ischemic heart failure.Liner correlation was used to analyze the relationship between Gal-3 and type I collagen,type III collagen as well as LVEF,respectively.5 Rabbit serum samples were collected before operation,2 weeks after operation and 6 weeks after operation respectively.Serum Gal-3 levels were detected by ELISA method.Liner correlation was used to analyze the relationship between serum Gal-3 and LVEF,respectively.6 Six weeks after operation,infarct tissues of rabbits were taken out.HEstaining and Masson staining were used to detect the myocardial fibrosis in rabbit with ischemic cardiac dysfunction.Results:1 Compared with the sham group,the LVEF decreased significantly(P<0.05)and the LVEDD increased significantly(P<0.05)in cardiac dysfunction group at 6 weeks after operation.Rabbits with LVEF<50%measured with echocardiography 2 weeks after operation indicated that model was made successfully.2 Compared with the sham group,the expression of Gal-3 mRNA and protein in cardiac dysfunction group increased(P<0.05)at 6 weeks after operation.At the same time,the expressions of type I collagen and type ?collagen mRNA and protein content also increased(P<0.05).3 Compared with the sham group,the concentration of Gal-3 in the serum was significantly increased at 2 and 6 weeks after the operation in cardiac dysfunction group.(P<0.05).4 Pathological results: Compared with the sham group,the myocardial cell structure of the cardiac dysfunction group was completely destroyed,the shape and size were different,the arrangement was disorderly,and the fibrous tissue was accumulated.5 Correlation analysis: The mRNA level of Gal-3 in infarct area was positively correlated with the mRNA level of type I collagen and type III collagen(r=0.948,P<0.05;r=0.913,P<0.05)and was a negatively correlated with LVEF(r =-0.919,P <0.05).The protein level of Gal-3 in infarct area was positively correlated with the protein level of type I collagen and type III collagen(r =0.907,P<0.05;r =0.925,P<0.05)and was a negatively correlated with LVEF(r =-0.909,P<0.05).The serum Gal-3 was a negatively correlated with LVEF(r =-0.940,P <0.05).Conclusion:1 This study confirmed the simultaneous functional and structural remodeling in ischemic cardiac dysfunction rabbits.2 Gal-3 participated in the process of myocardial fibrosis in ischemiccardiac dysfunction rabbits and promotes ventricular remodeling and heart failure.3 The level of Gal-3 was negatively correlated with the cardiac function in rabbits with ischemic cardiac dysfunction.With the level of Gal-3increasing,the heart function of rabbits was decreased.
Keywords/Search Tags:Galectin-3, Cardiac Dysfunction, Myocardial Infarction, Ventricular Remodeling, Myocardial Fibrosis
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