大豆异黄酮对阿霉素致心衰大鼠心功能的影响

Effect of soybean isoflavones on heart function of rats with adriamycin-induced heart failure

目的 :观察大豆异黄酮 (soybeanisoflavones ,SI)对阿霉素 (adriamycin ,ADR)致心力衰竭大鼠心功能的影响。 方法 :取成年雄性SD大鼠 30只 ,随机分为空白对照组、阿霉素组及大豆异黄酮低、中、高剂量组 ,每组 6只。大豆异黄酮低、中、高剂量组分别予SI 30、6 0、12 0mg·kg 1·d 1灌胃 ,1次 /d ,连续 6d ;其他两组灌注等量生理盐水。第 7天除空白对照组外 ,其余 4组一次性腹腔注射盐酸阿霉素 10mg/kg ,复制急性心衰大鼠模型 ,利用MedLab U/ 4c生物信号采集处理系统采集心室内压并分析。电镜观察心肌细胞超微结构变化。结果 :与对照组相比 ,阿霉素组左室收缩峰压 (LVSP)、室内压最大上升速率(+dp/dtmax)、室内压最大下降速率 (-dp/dtmax)、心肌纤维收缩成分缩短速度的最大值 (Vpm)显著降低 (P <0 .0 1) ;与阿霉组相比 ,高剂量大豆异黄酮组LVSP、±dp/dtmax和Vpm显著升高 (P <0 .0 5或P <0 .0 1)。电镜显示阿霉素组大鼠心肌细胞线粒体水肿、破裂、嵴消失 ,肌原纤维变性、溶解、大片坏死。闰盘间隙增宽 ,心肌间质纤维化。高剂量大豆异黄酮组 ,心肌肌原纤维病变明显减轻 ,部分排列紊乱 ,无坏死和溶解 ;部分线粒体水肿。结论 :高剂量大豆异黄酮可减轻阿霉素对心肌的毒性作用 。

Objective:To observe the protective effect of soybean isoflavones (SI) on the heart function of the rats with adriamycin-induced heart failure.Methods:Thirty adult male SD rats were divided into 5 groups:normal control (NC) group, adriamycin (ADR) group, L-SI group, M-SI group and H-SI group. SI of 30, 60, 120 mg·kg -1·d -1 was orally administered through a stomach tube once a day for 6 days in L-SI group, M-SI group and H-SI group, respectively. The other two groups were given the same amount of normal saline the same way. Then ADR of 10 mg/kg was given intraperitoneally once to copy the model of heart-failure. The MedLab-U/4c biological signal collecting system was used to record and analyze the LVSP of the rats. The pathological changes of the cardiomyocytes were observed. Results: As compared with NC group, the LVSP, ±dp/dt max, Vpm of the ADR group were significantly lower(P<0.05 or P<0.01), but those of the H-SI group were markedly higher than those of the ADR group (P<0.01). Electron microscopic morphometry of the heart samples of the rats in ADR group revealed typical alterations,consisting an increase of collagen content, vacuolation, diminishing of the cardiomyocyte diameter, alteration of myofilaments and Z-lines of myofibers, and myofibrillar degeneration. SI of 120 mg·kg -1·d -1 treatment could prevent the loss of myofibrillae and the reduction of myocyte diameter, and the degeneration of myofilaments and Z-lines were reversed by SI. Conclusion:SI of 120 mg kg· -1·d -1 treatment can relieve the toxic effect of ADR on myocardium, and also obviously improve the cardiac contractility of heart-failure rats.