人参Rb组皂苷对大鼠实验性心肌缺血再灌注损伤的保护作用

目的：观察人参Rb组皂苷（G-Rb）对大鼠实验性心肌缺血再灌注损伤的保护作用。方法：在体大鼠结扎冠状动脉前降支30 min，再灌注24 h制备实验性心肌缺血再灌注损伤模型，G-Rb按25、50和100 mg?kg^-1?d^-1给大鼠连续灌胃7 d，假手术组及再灌模型组灌胃0.5%羧甲基纤维素钠，计算心肌梗塞范围（MIS），测定血清天冬氨酸氨基转移酶（AST）、乳酸脱氢酶（LDH）、心肌型肌酸激酶同功酶（CK-MB）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性及丙二醛（MDA）含量，血浆前列环素（PGI₂）及血栓素A₂（TXA₂）水平，测定血小板聚集活性。结果：与再灌模型组比较，G-Rb 50、100 mg?kg^-1组大鼠的MIS缩小（P<0.05或P<0.01），血清AST、LDH、CK-MB活性及MDA含量降低（P<0.05或P<0.01），SOD及GSH-Px活性升高（P<0.05或P<0.01），血浆TXA2水平下降，PGI₂水平及PGI₂/TXA₂比值增高（P<0.05或P<0.01），1、3和5 min的血小板聚集率（PAR）及最大血小板聚集率（MPAR）降低（P<0.05或P<0.01）。结论：G-Rb对大鼠实验性心肌缺血再灌注损伤具有明显保护作用，可能与其增强抗氧化酶活性，减少自由基对心肌的氧化损伤，纠正PGI₂/TXA₂失衡以及抑制血小板聚集活性等机制有关。

Protective effects of Ginsenoside-Rb on experimental myocardial ischemia-reperfusion injury in rats

Objective To observe the protective effects of Ginsenoside-Rb(G-Rb)on experimental myocardial ischemia-reperfusion injury in rats.Methods The myocardial ischemia-reperfusion model was induced by 30 min left anterior descending coronary occulusion and 24 h reperfusion in openchest anesthetized rat.The changes of aspartate aminotransferase(AST),lactate dehydrogenase(LDH),MB isoenzyme of creatine kinase(CK-MB),superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)activities and malondialdehyde(MDA)content in serum,and prostacycline(PGI2)and thromboxane A2(TXA2)levels in plasma were determined.At the same time,the activity of platelet aggregation was also determined.Results In rats treated with G-Rb(with dose of 50 and 100 mg·kg-1 i.g for 7 d),the MIS was significantly reduced(P<0.05 or P<0.01),the AST,LDH and CK-MB activities in serum and the TXA2 level in plasma were declined(P<0.05 or P<0.01),while PGI2 level in plasma and PGI2/TXA2 ratio were increased signficatly(P<0.05 or P<0.01).In addition,the LPO content in serum was declined,SOD and GSH-Px activities in serum were increased markedly(P<0.05 or P<0.01).The platelet aggregation rate(PAR)at 1,3 and 5 min and maximum platelet aggregation rate(MOAR)were decreased markedly(P<0.05 or P<0.01).Conclusion G-Rb has protective effects on myocardial ischemia-reperfusion injury through improving free radicals metabolism,decreasing TXA2 level in plasma,increasing PGI2 level in plasma and PGI2/TXA2 ratio,and inhibitting the activity of platelet aggregation etc.