| Object:To study the effect of dioscin on platelet activation with myocardial ischemiareperfusion injury in rats,and the effects of dioscin on angiotensinⅡ(AngⅡ)-induced cardiomyocyte hypertrophy and the expression of some signal proteins.Methods:1.Male Wistar rats were randomly divided into 4 groups:IR group,dioscin low dose(150 mg/kg,D_L) group and dioscin high dose(250 mg/kg,D_H) group.Expression of CD62p,CD3 in platelet were measured by FCM and PAF with ELISA.2.Cultured cardiomyocytes of neonatal Wistar rats induced with AngiotensinⅡrandomly divided into five groups:Control group;I/R group;dioscin groups (10mmol/ml,20μmol/ml,40μmol/ml).The total protein of each group was determined by coomassie brilliant blue.The expressions of p38 and mitogen activated Protein Kinase Phosphatase-1(MKP-1) were assessed using Western blotting.Results:1.the effects of dioscin against myocardial ischemia reperfusion injury in rats: Compared with the MI/R group,the damage of the cardiomyocytes,the interstitial hemorrhage decreased in both the DL and the DH group And dioscin also reduce the myocardial swelling.Myocardium fracture was absent in the DL and DH group.The incidence of ventricular arrhythmia was 85.71%(I/R group)(85.71%),control group (0%),DL group(12.5%) and DH group(0%),compared with MI/R group(P＜0.01). No obvious difference was observed between DH and DL group.2.Expression of P-selectin(CD62p):Compared with the control group,the expression of the CD62p of MI/R group was increase significantly(9.23±3.06 vs 20.30±9.18%,p＜0.05),compared with MI/R group,the expression of CD62p in dioscin groups(L/H) decreased significantly.(20.30±9.18vs 12.15±4.65%, 20.30±9.18vs 10.01±3.05%,p＜0.05).There was no significant difference between the two dioscin groups.3.Expression of CD63:Compared with the control group,the expression of the CD63 of MI/R group was increase significantly(5.25±2.11 vs 18.72±7.14%,p＜0.05), compared with MI/R group,the expression of CD63 in DH group decreased significantly(18.72±5.14vs 14.79±4.13,p＜0.05).There was no significant difference between the DL group and the I/R group.4 Concentrations of platelet activating factor(PAF):Compared with the control group,the expression of the PAF of I/R group was increase significantly(8.2±2.34 vs 20.79±6.37 ng/ml,p＜0.05).compared with MI/R group,the expression of PAF in DH group decreased significantly(20.79±6.37vs 15.17±2.50,p＜0.05).There was no significant difference between the DL group and the MI/R group.5.The total Protein:Compared with the control group,the total protein of AngⅡgroup increased significantly(53.41±3.42vs 96.42±3.95,p＜0.01).Compared with AngⅡgroup,the total protein of all dioscin groups decreased significantly (63.27±1.56 vs 96.42±3.95,55.06±2.88 vs 96.42±3.95,50.50±1.41vs 96.42±3.95μg/w,p＜0.05).The total protein in DH,DM groups was same as that in control group.6.The expression of p38.Compared with the control group,the expression of p38 in AngⅡgroup increased significantly(182.75±10.44vs 114.07±8.36%,p＜0.01), Compared with the AngⅡgroup,the expression of p38 in all dioscin groups decreased significantly(160.36±17.29 vs 182.75±10.44,125.21±11.54 vs 182.75±10.44 120.90±9.25 vs 182.75±10.44%,p＜0.05).The expression of p38 in DH group was same as that in control group.7.The expression of mitogen-activated protein kinase phosphatase-1(MKP-1 Compared with the control group,the expression of MKP-1 in AngⅡgroup decreased significantly(64.24±6.71 vs 124.44±9.65%,p＜0.01),compared with the AngⅡgroup,the expression of MKP-1 in DM,DH groups increased significantly (118.12±9.04 vs 64.24±6.71,86.38±7.22 vs 64.24±6.71%,p＜0.05).Conclusions:1.Dioscin can reduce the platelet activation during myocardium ischemicreperfusion injury,prevent the information of thrombosis,protect the cardiac myocytes. 2.The anti-hypertrophic effects of dioscin on AngiotensinⅡ-induced cardiaomyocyte hypertrophy were associated with the inhinition of p38 pathway via regulation of MKP-1.
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