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Egg white-derived peptides decreased blood pressure via the competing endogenous RNA regulatory networks in female spontaneously hypertensive rats

ABSTRACT: Despite numerous studies reporting the effects and mechanisms of antihypertensive peptides including peptides derived from egg white proteins, the role of peptides in female hypertensive animal model is unknown. On the other hand, the role of epigenetic modulation by the peptide treatment has been rarely investigated. This study sought to investigate the effect of egg white protein hydrolysate (EWH) in female spontaneously hypertensive rats (SHRs) as well as to explore the underlying mechanisms from the perspectives of transcriptome and the profiles of non-coding RNAs. Young (12-14-week-old) female SHRs were orally administered with 250 mg/kg body weight (low-dose) or 1000 mg/kg body weight (high-dose) of EWH daily for 10 weeks. Blood pressure of the rats were monitored weekly. The miRNA in the aorta were profiled by the high-throughput RNA-seq technique. Differentially expressed (DE) RNAs in the aorta were identified for the construction of the competing endogenous RNA (ceRNA) networks and key molecules were validated by qRT-PCR. The treatment of the high-dose EWH showed a significant effect in reducing blood pressure in female SHRs. Bioinformatic analyses revealed 90 DE-miRNAs.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE242386 | GEO | 2024/12/31

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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Egg white-derived peptides decreased blood pressure via the competing endogenous RNA regulatory networks in female spontaneously hypertensive rats

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