目的观察黄芪总皂苷(AST)对心室重构大鼠血流动力学及抗氧化作用的影响。方法通过结扎大鼠左冠状动脉前降支4周建立实验性心室重构模型。将Wistar大鼠随机分成空白对照组、模型对照组、AST组和阳性对照组。AST组和阳性对照组分别灌胃给予AST100mg/kg和卡托普利100mg/kg,空白对照组及模型对照组灌胃给予等体积0.5%羧甲基纤维素钠溶液,每日1次,连续4周。4周后测定各组大鼠血流动力学;测量各组大鼠体重,左心室绝对重量,计算左心室相对重量;测定各组大鼠体内血清丙二醛(MDA)含量,血清超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性;测定各组大鼠心肌胶原含量及Ⅰ/Ⅲ胶原比例。结果AST能明显降低心室重构大鼠左心室舒张末压(LVEDP),升高平均动脉压(MAP)和左心室内压最大上升和下降速率(±dp/dtmax);减轻心室重构大鼠左心室绝对重量及相对重量;降低心室重构大鼠心肌间质胶原含量和Ⅰ型胶原/Ⅲ型胶原比例;降低心室重构大鼠血清MDA的含量,提高SOD和GSH—Px活性。结论AST对大鼠实验性心室重构具有保护作用,机制可能与其抑制心肌间质纤维化及增强机体抗氧化能力有关。
Objective To observe the effect of astragalosides(AST) on hemodynamics and antioxidation in ventricu lar remodeling rats. Methods The ventricular remodeling model was induced by myocardial infarction in rats of left an terior descending coronary occulusion. The wistar rats were divided into 4 groups,including Blank control group,model control group,AST group and positive control group (captopril). The rats in AST group and positive control group were treated with respectively AST 50mg/kg and captopril 100 mg/kg , the rats in sham operation group and model control group were treated with equal volume of 0.5% sodium carboxymethyl cellulose Solution, 1 times a day for 4 weeks. After 4 weeks,hemodynamics, body weight, left ventricular absolute weight and the relative weight of the left ventricle were measured; the serum malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity were measured; myocardial collagen content and Ⅰ/Ⅲ collagen ratio were measured in each group. Results AST could significantly reduce LVEDP of model group rats,increase MAP, ±dp / dtmax df model control group; AST could significantly reduce left ventricular absolute weight and the relative weight of the left ventricle model control group; AST could significantly reduce myocardial collagen content and Ⅰ/Ⅲ collagen ratio; AST could signifi- cantly decrease MDA content and increase the activity of SOD,GSH-Px. Conclusion AST has protective effect on ex- perimental ventricular remodeling , which mechanism may be related to inhibiting myocardial interstitial fibrosis and en- hance the body's antioxidant capacity.