| Objective: The aim of this study was to investigate the effects and mechanisms of rosuvastatin on ventricular remodeling,cardiomyocyte apoptosis by detecting the expressions of Bax, Bcl-2, Caspase-3,P38,p-P38 and the apoptosis index (AI) after myocardial infarction.Methods:45 male New Zealand albino rabbits were divided into three groups randomly: Group Rosuvastatin, rabbits were given rosuvastatin 10mg*kg-1*d-1 via direct gastric gavage within 24 hours after the ligation(Group R,n=15),group AMI , the animals was given normal saline as the same volume as group rosuvastatin(group MI, n=15), group sham-operation , rabbits received sham operation as health control and was administered with normal saline too( Group S,n= 15). Acutte myocardial infarction (AMI) models were made by the ligation of left anterior descending coronary artery(LAD). After two weeks, the effects of rosuvastatin were evaluated by detecting the changes of transthoracic echocardiography . After that,all the rabbits were killed and their hearts were taken out to detect left ventricular mass(LVM),LVMI(LVM/body mass), HE and Masson stained the tissue of the edge around the region of AMI . Terminal deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling (Tunel ) and flow cytometry were used to detect apoptosis index of the edge around the region of AMI, the protein expressions of Bax, Bcl-2, Caspase-3,P38,p-P38 were detected by the way of western blot.Results:(1)Animal models of AMI were established successfully(.2) Compared with group MI,the left ventricular end diastolic diameter (LVEDD) and left ventricular end systolic diameter (LVESD) was smaller significantly in group R(13.0±0.21mm vs 16.0±0.50mm p<0.01; 8.2±0.30mm vs 11.8±0.81mm p<0.01),but left ventricular ejection fraction (LVEF%) were significantly increased (0.66±0.05 vs 0.53±0.06,p<0.01),Compared with group S, LVEDD and LVESD were significantly increased(16.0± 0.50mm?14.2±0.41mm vs 13.0±0.21mm,p<0.01;11.8±0.81mm?9.85±0.34mm vs 8.2±0.30mm,p<0.01 )while LVEF was significantly decreased (0.53±0.06?0.66±0.05 vs 0.75±0.02,p<0.01)in group MI and group R.(3) Compared with group S,LVM and LVMI were increased( 3.49±0.33?3.96±0.34 vs 3.01±0.28,p<0.01)in group R and group MI,but LVM and LVMI in group R was decreased than those in group MI(3.49±0.33 vs 3.96±0.34,p<0.05).(4) Compared with group S,the collagen volume fraction(CVF%) of the edge around the region of AMI were higher significantly in group MI and group R(10.5±3.4?6.4±2.1 vs 3.3±1.2, p<0.01),the CVF in group R was decreased than those in group MI(10.5±3.4 vs 6.4±2.1, p<0.01).(5)Compared with group MI, the apoptosis index (AI) in the edge of myocardial infarction region of hearts were decreased significantly in Group R(p<0.01),(6) Compared with group S, the protein expressions of Bax/?-Actin?p-P38/?-Actin and casepase-3/?-Actin in group MI and group R were increased significantly(1.86±0.32?1.71±0.28 vs 1.01±0.02,p<0.01; 1.55±0.60?2.10±0.20 vs 0.98±0.03,p<0.01; 3.10±0.91?2.60±0.80 vs 0.97±0.05,p<0.01). there were no significant differences among Group R?Group MI and group S in the expression of P38,however, Compared with group MI, the protein expression of Bcl-2 was increased significantly in Group R(0.60±0.03 vs 0.20±0.01,p<0.05) .Conclusion:(1).Animal models of AMI were established by the ligation of left anterior descending coronary artery(LAD) in rabbits successfully. (2)Ttreatment with rosuvastatin can ameliorates early ventricular remodeling and improves cardiac function after AMI in albino rabbit models.(3) Rosuvastatin can reduce cardiomyocyte apoptosis in the edge of myocardial infarction region of the hearts,the mechanisms of which may be associated with down-regulating the protein expression of Caspase-3 and p-P38,and up-regulating the expression Bcl-2. |
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