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. 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. Diffusesed 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 detection 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 uniqu e 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. expression found 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 strongly 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 can facilitate our understanding of the pharmacological mechanisms of BYHWD in ventricular remodeling post-myocardial infarction.