Abstract

Low-salt(LS) always be abided as dietary principle by hypertension patients. However, recent studies found that the incidence of cardiopathy and stroke increases in subjects with LS diet(<3g/d), meanwhile, LS can accelerate the development of atherosclerosis. It is essential to study deeply on the relationship between the amount of salt intake and cardiovascular diseases. We performed an analysis to explore the possible molecular mechanism of salt-induced cardiovascular disease. Microarray datasets (GSE17149) of heart tissue from LS diet dogs was obtained from NCBI’s GEO Database. The data was analyzed by QOE, STRING and Genclip 2.0. The protein-protein interactions (PPI) networks of the differentially expressed genes(DEGs, p<0.05, q<0.05, Fold change>2) between the LS group and control group (normal diet) were conducted to screen the key biomarkers between the two groups. Compared with the control group, the gene expression profile of heart tissue from dogs was changed in the LS group(0.05% of sodium chloride, approximately 150 mg/d). 1343 (3.12%) DEGs were found from 43035 genes in total. The results also revealed that NFKBIA and NR1H2 were the cores of the PPI networks, which were mainly related to reduce the function of macrophage-derived foam cells and to promote cholesterol discharge and decomposition. The signaling pathways such as MAPK, PI3K-Akt, NF-kappa B were activated when the dogs received LS diet, which resulted in lower risk of cardiovascular disease through anti-apoptosis, anti-inflammation, anti-oxidative stress, et al. The gene expression of heart tissue in LS diet dogs is significantly changed and LS diet may reduce the risk of cardiovascular disease by up-regulating the expression of NFKBIA, NR1H2 and oxidative stress-related signaling pathways. More rigorous and independent experiments are needed to validate the conclusions of the present study.

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