中文摘要：

目的观察他达拉非对阿霉素所致心肌病的保护作用及其作用机制。方法随机分为3组：模型组与实验组（均n=16）：一次性腹腔内注射阿霉素15mg·kg^-1制备小鼠心肌病模型。正常组（n=10）：一次性腹腔注射相同容量的生理盐水。在此基础上，实验组灌胃他达拉非4mg·k^-1，每日1次，共14天。给药2周后，进行心脏超声检查、光镜下观察及检测各组心肌组织中cGMP含量等。结果2周后，实验组与模型组左室舒张与收缩末期内径分别为（3．07±0．10）VS（3．50±0．20）mm与（2．17±0．10）VS（2．82±0．17）mm；左室射血分数分别为（57．85±2．03）％，（46．07±2．96）％；左室短轴缩短率分别为（29．20±3．05）％，（19．41±2．59）％；心肌细胞直径分别为（14．24±0．39），（13．78±0．36）μm；心肌纤维化面积比率分别为（2．35±0．21）％，（5．16±0．36）％；cGMP含量分别为（0．15±0．01），（0．05±0．01）Pg·mg^-1，2组比较均有统计学意义（均P〈0．05）。实验组的肌凝蛋白重链、肌钙蛋白I以及肌间蛋白的表达较模型组均明显升高。细胞凋亡各组间未见明显差异。结论他达拉非可能通过cGMP通路减轻阿霉素所致的心肌细胞萎缩和心肌纤维化，明显改善左心室功能障碍。

英文摘要：

Objective To study the protective effects and its mechanisms of tadalafil on doxorubicininduced cardiomyopathy in mice. Methods Mice were randomly assigned to three groups： model and test group（both n = 16）： a single intraperitoneal injection of doxorubicin 15 mg·kg^-1 to induce cardiomyopathy;normal group （n = 10） ： a single intraperitoneal injection of same volume of saline. On that basis, test group was treated with tadalafil 4 mg·kg^-1 , once a day, for 14 days, orally viagauge. After two weeks, echocardiograms were then recorded, histological analysis and the cardiac cGMP level were detected. Results Two weeks later, indicators of test group and model group were as follows ： left ventricular end - diastolic dimension were （ 3.07 ± 0.10 ）, （ 3.50 ± 0. 20） mm ; left ventricular end - systolic dimension were （2. 17 ± 0. 10）, （2. 82 ± 0. 17）mm; left ventricular ejection fraction were （57.85 ± 2. 03 ） %, （46. 07 ± 2. 96 ） % ; left ventricular percent fractional shortening were （29.20 ± 3.05 ） %, （ 19.41 ± 2. 59 ） % ; the transverse diameter of cardiomyocytes were（ 14.24± 0. 39 ）, （ 13.78±0.36 ） μm ; cardiac fibrosis were （ 2.35± 0. 21 ） %, （ 5.16 ± 0. 36 ） % ; the levels of cGMP were（0. 15 ± 0. 01 ） , （0.05 ± 0. 01 ） pg · mg^-1 There were significiant compared with model group （P 〈 0. 05 ）. The myocardial expression of myosin heavy chain, troponin I and desmin were significantly increased in the test group. No significant difference apoptotic effects were seen between each group. Conclusion The protective effects of tadalafil against doxorubicin - in- duced cardiomyopathy, mitigatting doxorubicin - induced impairment of cardiac function in mice, significantly attenuatting doxorubicin - induced atrophic degeneration of cardiomyocyte and myocardial fibrosis through possible activating cGMP signaling pathway.