中文摘要：

ObjectiveTo 在室的改变在基因表示上调查 Buyanghuanwu 煎(BYHWD ) 的效果在心肌的梗塞的 rats.MethodsAnimal 模型的 myocardial 以后梗塞被左前面的下降冠的动脉的永久结扎建立。 Echocardiography 大小在 BYHWD 的处理以后被执行( 18 g ?????????????????????吠?呑?牴慥浴湥?潃据畬楳湯楅桴牥?剔元???????吠?呑???????????吗????????????????渠略潲牰瑯'虡N敶？？

英文摘要：

OBJECTIVE： To investigate the effect of Buyanghuanwu decoction（BYHWD） on gene expression in ventricular remodeling post-myocardial infarction in rats.METHODS： Animal models of myocardial infarction were established by permanent ligation of the left anterior descending coronary artery. Echocardiography measurements were performed after the treatment of BYHWD（18 g·kg-1 collagen was observ·d-1） for 90 days.Myocardialed by mallory trichrome staining. Capillary density was quantified by using Factor rentially expⅧre immunohistochemical staining.Diffessed genes were explored by a short-read sequencing technology combined with a tag-based digital gene expression profiling（DGE）system. Real-time quantitative polymerase chain reaction detecting system（q PCR） was used to validate the sequencing results. After assembling the gene information from Sham, model and BYHWD groups, we constructed three DGE libraries based on each group. The sequencing of three libraries generated 66 000-73 000 unique tags, which were mapped to reference sequences for annotation of expressed genes.RESULTS： Among them, 511 and 352 differentially expressed genes were found in comparison with sham/model and model/BYHWD, respectively. Fifty-five genes exhibited reversed direction of gene expression differences between Sham/Model and Model/BYHWD groups. We found that transforming growth factor beta receptor-1, junctophilin-2,monocyte chemotactic protein 1, neuropeptide Y,arachidonate 5-Lipoxygenase, arachidonate 15-Lipoxygenase were significantly modulated, which suggested the involvement of these genes in BYHWD treatment.CONCLUSION： The DGE profiling data provide comprehensive gene expression information at the transcriptional level that could facilitate our understanding of the pharmacological mechanisms of BYHWD in ventricular remodeling post-myocardial infarction.