Characterization of the Effects of Oxymatrine on Myocardial Hypertrophy in SHR Through Metabolome and Transcriptome

Cardiac hypertrophy is a cardiac structural remodeling and dysfunction resulting from chronic hypertension and is an independent risk factor for cardiovascular morbidity and mortality. Study have implicated the protect role of oxymatrine (OMT) on the ventricular remodeling in spontaneously hypertensive rats (SHRs). However, the underlying mechanisms of remains unclear. In this study, we investigated investigates the potential of OMT in improving myocardial hypertrophy in SHRs through integrated analysis of transcriptomics and metabolomics. The results show that OMT significantly alleviates myocardial hypertrophy in SHRs and improves heart function by reducing the myocardial enlargement and collagen deposition. Transcriptomic analysis revealed that OMT reversed the expression of 10 genes associated with linoleic acid/arachidonic acid metabolism, cytochrome P450, steroid hormone biosynthesis, and myocardial adrenergic signaling. Metabolomic analysis indicated that OMT reversed the levels of 16 metabolites related to steroid hormone biosynthesis, aldosterone synthesis and secretion, and tryptophan metabolism. Integrated analysis revealed that Integrated analysis identified Cyp2e1 and desoxycortone (also known deoxycorticosterone, DOC) as key genes and metabolites involved in the transcriptional and metabolic interactions through which OMT improves myocardial hypertrophy in SHR. In summary, our study underscores the potential molecular and metabolic mechanisms of OMT against pressure overload-induced myocardial hypertrophy and provides theoretical support for its exploration in other indications. Comparative gene expression profiling analysis of RNA-seq data for the left ventricle in spontaneously hypertensive rats (SHR) with or without oxymatrine.