黄芪多糖对阿霉素诱导的心力衰竭模型大鼠的保护作用

目的 探讨黄芪多糖对大鼠阿霉素性心衰的保护作用。方法 取雄性SD大鼠30只，随机分为对照组、心衰模型组和黄芪多糖组，每组10只。黄芪多糖组连续14d黄芪多糖水溶液灌胃［3g/(kg·d)］，正常对照组和心衰模型组灌胃等量蒸馏水。心衰模型组和黄芪多糖组分4次静脉注射阿霉素［10.4mg/(kg·2d)］复制心衰模型。给药全部结束后，检测大鼠心肌重构、细胞凋亡和抗氧化性等指标。结果 阿霉素导致心肌纤维化，肌原纤维溶解断裂，线粒体肿胀变性，应用黄芩多糖能明显改善心衰症状。血流动力学和TUNEL染色进一步证实黄芪多糖能缓解阿霉素对心脏的损伤，这一作用可能是通过降低丙二醛(MDA)含量和Bax的表达，同时增加超氧化物歧化酶（SOD）活性和Bcl-2的表达来实现的。结论 黄芪多糖对阿霉素性心衰有较好的保护作用。

Protective effect of astragalus polysaccharides in model rats of doxorubicin induced cardiac injury

Objective To determine the protective effect of astragalus polysaccharides (APS) in doxorubicin induced heart faiure（HF）. Methods Thirty male Sprague-Dawly rats were randomly divided into three groups: control group, HF group and APS group. APS group received APS ［3g/(kg〖DK〗·d］for 14 days. HF group and APS group received doxorubicin 10.4mg/kg every 2 days for 4 times. Ventricular remodeling,apoptosis, and antioxidant indices were examined after the last intragastric administration. Results APS protected heart from myocardial fibrosis, myofibrils dissolve and broke, and mitochondria swelling. Evident cardiac damage induced by doxorubicin was revealed by hemodynamic changes and TUNEL staining compared to the control group. APS treatment caused significant attenuation of malonyldialdehyde（MDA）and Bax express. Superoxide dismutase (SOD) activity and Bcl-2 expression were significantly increased by APS in heart failure rats. Conclusion APS decreases doxorubicin-induced cardiotoxicity.