目的: 研究扩心方对阿霉素诱导扩张型心肌病模型大鼠心功能、心肌损伤的保护作用，探讨扩心方作用机制。方法: 50只Wistar大鼠腹腔注射阿霉素6周建立DCM模型，开始造模4周后随机分为模型组，扩心方高、中、低剂量组，卡托普利组（每组各10只），连续灌胃给药四周，另设10只正常对照。正常组和模型组以生理盐水灌胃。治疗结束后，对各组大鼠进行心脏超声检查，病理形态学检测，以及用反转录-聚合酶链反应和蛋白质免疫印迹法分别检测心肌组织中SERCA2α、PLB的mRNA和蛋白含量。结果: 与正常对照组相比, 模型组心功能减弱，出现心肌病理损害，SERCA2α与PLB表达异常；与模型组相比，扩心方组可以改善DCM大鼠的心功能、心肌病理学形态，同时，提高SERCA2αmRNA和蛋白表达、抑制PLB mRNA和蛋白表达。结论: 扩心能提高DCM大鼠的左心室射血分数和缩短率，减轻心肌损伤，改善心功能，同时调控DCM大鼠SERCA2α、PLB的表达。提示扩心方改善DCM大鼠心功能的作用机制，可能与纠正心肌肌浆网钙调控相关蛋白-SERCA2α、PLB的异常表达相关。

This paper was aimed to study the protective effect of Kuoxinfang (KXF) on heart function and myocardial injury in rats with adriamycin-induced dilated cardiomyopathy (DCM), and to explore its possible mechanism. Models of DCM were established by adriamycin injected via intraperitonealy for 6 weeks in 50 Wistar rats. After injected 4 weeks, models of DCM rats were randomly divided into the DCM group, the high-, medium-, and low-dose KXF group, and the captopril group (with ten rats in each group). Intragastric administration of the drug was given for four weeks. Another ten rats were used as normal control. Intragastric administration of physiological saline was given to rats in both the normal control group and DCM group. After treatment, all rats were examined by echocardiography and pathomorphology, while mRNA and proteins of SERCA2α and PLB in cardiac muscles were determined by methods of RT-PCR and Western blotting, respectively. The results showed that compared with the normal control group, cardiac function of the DCM group was weakened, the myocardial pathological damage appeared, and expressions of SERCA2α and PLB were abnormal. Compared with the DCM control group, KXF can improve cardiac function and myocardial pathomorphological changes. Meanwhile, KXF could increase the expression of SERCA2α and inhibit the expression of PLB in both mRNA and protein. It was concluded that treatment with KXF can not only effectively improve EF and FS of DCM rats, protect myocardium and improve heart function, but also partially regulate protein expressions of SERCA2α and PLB in DCM rats. The mechanism of KXF in treating DCM rats may be correlated with normalizing protein levels of calcium regulation-associated protein of myocardial sarcoplasmic reticulum, such as SERCA2α and PLB.

国家科学技术部科技支撑计划项目（2012BAI41B05）：慢性非传染性疾病防控领域中医预防保健（治未病）服务技术应用示范，负责人：周端；上海中医药大学中西医结合学科建设项目（2017）：中西医结合心血管疾病防治，负责人：刘萍，王佑华。