The Research About The Effects Of Rosuvastatin On Ventricular Remodeling In Rats With Myocardial Damage Induced By Isoprenaline

BackgroundVentricular remodeling is a kind of reaction of myocardium on myocardial injuryand overworked heart, including the size of ventricular, the changes of morphologyas well as organizational structure, and it is a complex pathophysiological process,with the main performance of cardiomyocyte hypertrophy, intercellular substancefibrosis, ventricular dilatation, which can result in ventricular systolic and diastolicdysfunction, progressive decline in cardiac function, eventually progress to heartfailure. Heart failure is a common terminal stage of cardiovascular disease, and howto slow down or delay the progress of ventricular remodeling is a hot spot in the fieldof cardiovascular disease treatment. Furthermore, according to current continuousresearches, the excessive expression of Galectin-3in myocardial cells has a closerelationship with the development of ventricular remodeling.HMG-CoA reductase inhibitors--statins, except for its lipid function, someother functions of cardiovascular protection like anti myocardial fibrosis, plateletaggregation and thrombosis and stable plaques have attracted much attention in recentyears. Currently,statins is not only used for the treatment of coronary atheroscleroticheart disease, it is also widely used to treat myocardial injury and reduce heart failure,however, whether its effect and mechanism of action can effectively interfere with the ventricular remodeling is still to be defined.ObjectiveThis research is to explore the method of establishing a rat model of myocardialinjury,the expression and changes of Galectin-3in myocardial injury of ratmyocardial cells, and to observe whether Rosuvastatin has the function of myocardialprotection, preventing or alleviating the effect of ventricular remodeling, which canprovide the basis for clinical application.MethodsDivide30healthy Wistar rats into3groups randomly and each group has10rats:Group A for myocardial injury model group, intraperitoneal injection of isopropyladrenaline200mg/kg,2times a day,5days in a row. Group B for Rosuvastatinintervention group, intraperitoneal injection of isopropyl adrenaline like Group A, onehour later, give them gastric drug lavage with5mg/kg Rosuvastatin dissolved in2mlof clean water (5days later, give gastric drug lavage at the same time). As the normalcontrol group, group C are given corresponding amount of saline injections. Group Aand C are given water lavage in relevant with group B. Five days later, take tailvenous blood detection of CK and LDH, and judge the model preparation and theintervention effect of injury by Rosuvaststin.6weeks is the end of the experiment,calculateventricular weight index, apex tissue for HE staining, and RT-PCR detectionof myocardial cell Galectin-3mRNA content changes, immunohistochemical stainingof judging myocardial cell Galectin-3expression, evaluate effects on ventricularremodeling by Rosuvastatin.ResultsSerum enzymology: CK and LDH in Group A and Group B were significantlyhigher than those in Group C, the difference had statistically significance (P <0.05),and CK and LDH in Group A was higher than those in group B (P <0.05). Rat ventricular weight index in Group A and B were significantly larger thanthose in Group C (P <0.05), and the comparative difference in Group A and Group Bcomparative difference had statistically significance (P <0.05).HE staining results: The myocardial tissue in Group A showed myocardial celledema fibrosis, disordered arrangement of myocardial fibers, fiber tissue hyperplasia,myocardial cell edema in Group B was lighter, myocardial fibers arranged relativelyneatly, law of myocardial fibers in Group C were arranged neatly form clear stripes,nucleus, cell with no swelling.RT-PCR: Myocardial cell Galectin-3mRNA expression in Group A was higherthan that in Group B (P <0.05), the difference had statistically significance (P <0.05).Immunohistochemical staining result: Galectin-3expressed less in group C; Ratmyocardial cell of Group A contained a lot of Galectin-3expression, compared withGroup A, there was less in Group B (P <0.05).ConclusionIsopropyl adrenaline can effectively induce formation of rat model of myocardialinjury, resulting in the ventricular remodeling changes.According to the increased expression of Galectin-3in myocardial injury modelof rats myocardial cells, it can be inferred that Galectin-3plays an important role inmyocardial injury and ventricular remodeling as well as the process of the occurrenceand development, and the increased levels reflect the progression of ventricularremodeling to a certain extent.Rosuvastastin can effectively intervene myocardial injury rat ventricularremodeling, the improvement of ventricular remodeling mechanism may be related tothe inhabitation of Galectin-3myocardial cells and then reducing myocardial fibrosis.