摘要目的:探讨二氢杨梅素（DHM）对多柔比星所致心肌损伤的保护作用及其作用机制。方法:24只健康雄性SD大鼠分为4组：对照组、多柔比星组、多柔比星+DHM 100组、多柔比星+DHM 200组。第6周末麻醉处死大鼠，超声心动图检测大鼠心功能；通过HE染色、Masson染色、WGA染色观察大鼠心肌组织形态学变化；脱氧核糖核苷酸末端转移酶介导的原位缺口末端标记（TUNEL）观察心肌细胞凋亡情况；Western blot和免疫组织化学方法检测NLRP3、caspase-1、白细胞介素（IL）-1β、bax、bcl-2蛋白水平。结果:与对照组相比，多柔比星组左心室射血分数和左心室短轴缩短分数明显下降，收缩期左心室内径和舒张期左心室内径明显增加；与多柔比星组相比，多柔比星+DHM组左心室射血分数和左心室短轴缩短分数均上升，收缩期左心室内径和舒张期左心室内径均下降（ P<0.05）。组织学发现，多柔比星组出现明显的心肌损伤表现，而多柔比星+DHM组显著抑制了多柔比星引起的大鼠心肌损伤。同时，在多柔比星组出现了明显的心肌细胞肥大，而多柔比星+DHM组显著抑制了心肌细胞肥大。与对照组相比，多柔比星组心肌细胞凋亡水平、bax/bcl-2比值增加，而多柔比星+DHM组心肌细胞凋亡明显受到抑制（ P<0.05）。此外，与对照组比较，多柔比星组NLRP3、caspase-1、IL-1β水平升高（ P<0.05）；而多柔比星+DHM组NLRP3、caspase-1、IL-1β水平明显降低（ P<0.05）。 结论:DHM通过抑制NLRP3炎症小体，改善心肌细胞凋亡，对多柔比星所致大鼠心脏损伤起到保护作用。

abstractsObjective:To investigate the protective effect of dihydromyricetin (DHM) on doxorubicin (DOX)-induced myocardial injury and its mechanism.Methods:Twenty-four healthy male SD rats were divided into 4 groups: control group, DOX group, DOX+DHM100 group and DOX+DHM200 group. Echocardiography was used to measure cardiac function. At the end of the 6th week, the rats were anesthetized and sacrificed, and the pathological changes of the cardiac tissues were observed by HE staining, Masson staining and WGA staining. Cardiomyocyte apoptosis was observed by TUNEL staining, and protein levels of NLRP3, caspase-1, IL-1β, bax and bcl-2 were detected by Western blot and immunohistochemistry.Results:Compared with the control group, the left ventricular ejection fraction and left ventricular fractional shortening decreased significantly in DOX group, while left ventricular internal dimension at systole and left ventricular internal dimension at diastole increased. In DOX+DHM group, both left ventricular ejection fraction and left ventricular fractional shortening increased, while left ventricular internal dimension at systole and left ventricular internal dimension at diastole decreased ( P<0.05). Furthermore, DOX group showed significant myocardial injury histologically, while DOX+DHM group significantly inhibited DOX-induced myocardial injury in rats. Meanwhile, cardiomyocyte hypertrophy was found in the DOX group, while the cardiomyocyte hypertrophy was notably inhibited in the DOX+DHM group. Compared with the control group, the apoptotic rates of cardiomyocytes and the levels of bax/bcl-2　ratio were significantly increased in DOX group, which were significantly alleviated in the DOX+DHM group ( P<0.05). In addition, the levels of NLRP3, caspase-1 and IL-1β were increased as compared with control group, while the levels of the above indicators were remarkably reversed in DOX+DHM group as compared with DOX group ( P<0.05). Conclusion:DHM alleviates DOX-induced myocardial injury in rats by inhibiting NLRP3 inflammasome and reducing cardiomyocyte apoptosis.