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

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE282767 | GEO | 2025/09/26

REPOSITORIES: GEO

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Project description:Abstract Background: Long-term hypertension can lead to hypertensive heart disease, which ultimately progresses to heart failure. As an angiotensin receptor blocker (ARB) antihypertensive drug, allisartan can control blood pressure and improve cardiac remodeling and cardiac dysfunction caused by hypertension. The objective of this study is to investigate the protective effects of Allisartan on the heart of spontaneously hypertensive rats (SHRs) and the underlying mechanisms. Methods: We used spontaneously hypertensive rats (SHRs) as an animal model of hypertensive heart disease and treated them with allisartan orally at a dose of 25 mg/(Kg·day). We continuously monitored the rats' blood pressure levels, measured their body and heart weights, and evaluated their cardiac structure and function using echocardiography. WGA staining and Masson trichrome staining were employed to assess the morphology of the myocardial tissue. We performed transcriptome and proteome analysis using the Solexa/Illumina sequencing platform and tandem mass tag (TMT) technology, respectively. We used immunofluorescence co-localization to analyze Nrf2 nuclear translocation, and TUNEL to detect the level of cell apoptosis. The protein and mRNA levels were determined by Western blotting and qRT-PCR, respectively. Results: Allisartan lowered blood pressure, attenuated cardiac remodeling, and improved cardiac function. Allisartan alleviated cardiomyocyte hypertrophy and cardiac fibrosis. Allisartan significantly affected the pentose phosphate pathway, fatty acid elongation, valine, leucine and isoleucine degradation, glutathione metabolism, and amino sugar and nucleotide sugar metabolism pathways in the hearts of SHRs, and upregulated the expression level of GSTM2. Allisartan activated the PI3K-AKT-Nrf2 signaling pathway and inhibited cardiomyocyte apoptosis. Conclusions: Our study determined that allisartan effectively controls blood pressure in SHRs and improves cardiac remodeling and cardiac dysfunction. Allisartan upregulates the expression level of GSTM2 in the hearts of SHRs and significantly affects glutathione metabolism shown by transcriptomics and proteomics analysis. The cardioprotective effect of allisartan may be mediated through activation of the PI3K-AKT-Nrf2 signaling pathway, upregulation of GSTM2 expression, and reduction of SHRs cardiomyocyte apoptosis.

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

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