中文摘要：

识别 Dingxin 的保护的效果的内在的机制的目的配方(：， DXR ) ，在中国临床上被使用超过 20 年了的一张中国复合药方，在 ischemia/reperfusion (I/R ) 上，在老鼠的导致的心律不齐当模特儿。

英文摘要：

Objective： To identify the underlying mechanisms of the protective effects of Dingxin Recipe （定心方, DXR）, a Chinese compound prescription that has been used clinically in China for more than 20 years, on ischemia/reperfusion （I/R）-induced arrhythmias in rat model. Methods： A total of 30 rats were randomly divided into three groups： sham group, I/R group, and DXR-pretreated I/R （DXR-I/R） group. Rats in the DXR- I/R group were intragastrically administrated with DXR （12.5 g/kg per day） for consecutive 7 days, while rats in the sham and I/R groups were administrated with normal saline. Arrhythmias were introduced by I/R and electrocardiograms （ECG） were recorded. Two-dimensional （2-D） polyacrylamide gel electrophoresis and matrix- assisted laser desorption ionization time-of-flight mass spectrometry （MALDI-TOF MS） were used to identify differentially expressed proteins. Immunohistochemistry, real-time quantitative polymerase chain reaction （RQ- PCR）, Western blot, and enzyme-linked immunosorbent assay （ELISA） were performed to analyze proteins obtained in the above experiments. Results： DXR significantly reduced the incidence and mean duration of ventricular tachycardia and ventricular fibrillation and dramatically decreased the mortality, as well as arrhythmia score, compared with those of the I/R group. Among successfully identified proteins, prohibitin （PHB） and heart fatty acid binding protein （hFABP） were up-regulated in DXR-pretreated I/R rats compared with those of the I/R rats. In addition, compared with the I/R group, the level of glutathione （GSH） was elevated accompanied by reduced expressions of interleukin-6 （IL-6） and neutrophil infiltration in I/R rats with DXR pretreatment. Conclusions： DXR could alleviate I/R-induced arrhythmias, which might be related to increased expression of PHB. The enhanced expression of PHB prevented against the depletion of GSH and consequently inhibited apoptosis of cardiomyocytes. Furthermore, up-regulation