Abstract: Objective To investigate the mechanism by which Siwei Tumuxiang powder ameliorates hypertensive myocardial hypertrophy so as to provide a reference for clinical treatment. Methods A rat model of myocardial hypertrophy was established via abdominal aortic ligation. Transcriptomics technology and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were used. Eighteen Sprague-Dawley (SD) rats were randomly divided into three groups: the sham-operated group (Sham), the model group (Mod), and the Siwei Tumuxiang powder administration group (STP, 1.6 g·kg^-1·d^-1), with six rats in each. A model of hypertensive myocardial hypertrophy was constructed via abdominal aortic coarctation in the Mod and STP groups. The STP group was given STP solution by gavage at a dose of 1.6 g·kg^-1·d^-1, while the Sham and Mod groups received an equal volume of normal saline by gavage. After 8 weeks of feeding, echocardiography was used to evaluate the cardiac function of each group. Heart tissue sections were stained with HE and Masson to observe the pathological changes in the structure of myocardial tissue and the degree of myocardial fibrosis. Western blot was used to detect the expressions of hypertrophy-related proteins. Based on network pharmacology simulation, a component-target network map was constructed and pathway enrichment analysis was conducted to predict the potential biological pathways of Siwei Tumuxiang powder against hypertensive myocardial hypertrophy. RNA-Seq was used for sequencing to analyze the differentially expressed genes, which were subjected to GO and KEGG enrichment analysis. The expressions of target genes were verified by qPCR. Results Echocardiography showed that the AWT and PWT of the STP group were significantly reduced, while EF and FS were significantly increased. HE and Masson staining suggested that Siwei Tumuxiang powder could mitigate the disordered arrangement of myocardial cells, cell hypertrophy, inflammatory infiltration, and the appearance of obvious fibrotic areas around myocardial vessels and in myocardial tissue spaces. Western blot showed that the expressions of hypertrophy-related protein ANP and fibrosis-related protein COL-1 were inhibited. The results of network pharmacology indicated that the 150 main components in Siwei Tumuxiang powder might exert therapeutic effects against hypertensive myocardial hypertrophy through 124 potential core targets. RNA-Seq identified 1 168 differentially expressed genes between the Sham group and the Mod group, and another 47 between the Mod group and the STP group. There were 22 feedback expressed genes in the intersection, among which 3 differentially expressed genes were related to hypertensive myocardial hypertrophy: Hamp, Ndrg1, and Gfpt2. RT-qPCR showed that Siwei Tumuxiang powder could reverse the expressions of Hamp, Ndrg1, and Gfpt2 genes in the heart tissue of model rats of hypertensive myocardial hypertrophy. Conclusions iwei Tumuxiang powder can retard the occurrence and development of hypertensive myocardial hypertrophy by regulating Hamp, Ndrg1, and Gfpt2 genes through complement and coagulation cascade, PPAR signaling pathway, and cholesterol metabolism pathways.

Key words: Hypertensive Myocardial Hypertrophy, Siwei Tumuxiang Powder, Transcriptomics, Coagulation Cascade, PPAR Signaling Pathway, Cholesterol Metabolism Pathways, Rats