Physical exercise protects muscle from accelerated aging induced by high-salt intake and muscle CG2196(salt)gene overexpression in Drosophila

Aging decreases muscle mass,strength,and functional capacity.High-salt stress seems to promote muscle aging and decrease lifespan.However,exercise delays muscle aging and increases longevity,and it may protect muscle from rapid aging induced by high-salt intake(HSI),but the molecular mechanisms are poorly understood.In this study,the flies were fed a high-salt diet and trained to exercise.Muscle CG2196(salt)gene and dSir2 gene were over-expressed by building mef2-gal4/UAS system.The results showed that both physical exercise and muscle dSir2 gene overexpression prevented HSI-induced and muscle salt overexpression-induced accelerated age-related decline of climbing index,climbing endurance,muscle NAD^(+)level,SOD activity level,dSir2 expression,and dFOXO expression,and they also prevented HSI-induced and muscle salt overexpression-induced accelerated age-related increase in muscle ROS level,MDA level,and salt gene expression.Physical exercise improved lifespan decrease induced by HSI and muscle salt overexpression.Therefore,current results indicated that high-salt stress accelerated muscle aging by decreasing muscular NAD^(+)/dSir2/dFOXO pathway activity and increasing oxidative stress.Physical exercise protected muscle from accelerated aging induced by high-salt stress through activating muscle NAD^(+)/dSir2/dFOXO pathway and enhancing muscle oxidation resistance.The combination of exercise and muscle dSir2 overexpression had the best protective effect on muscle aging and lifespan in flies.

Selenium-enriched and ordinary green tea extracts prevent high blood pressure and alter gut microbiota composition of hypertensive rats caused by high-salt diet

High-salt diet is well recognized as a risk factor for hypertension,and dietary intervention plays a critical role in the prevention of hypertension.The current study investigated the effects of selenium-enriched green tea(Se-GT)and ordinary green tea(GT)on prevention of hypertension of rats induced by high-salt diet,as well as their potential regulatory and mechanism.Our results showed that GT and Se-GT supplementations significantly prevented the increase of blood pressure(BP),activated the phosphoinosmde-3-kinase/protein kinase B(PI3K/Akt)signaling pathway,and regulated the gene expression related to BP,as well as improved the tissue damage like heart,liver,and kidneys.Besides,the key parameters associated with oxidative stress,inflammation and endothelial dysfunction were also altered by GT and Se-GT treatments.Importantly,GT or Se-GT administration adjusted the diversity and composition of the intestinal flora.Moreover,GT and Se-GT supplementations increased the abundance of beneficial bacteria and reduced the abundance of harmful or conditional pathogenic bacteria.More specifically,GT intake specifically and significantly enriched the relative abundance of Paraprevotella and Bacteroides,whereas Se-GT was characterized by specific and significant enrichment for Allobaculum and Bifidobacterium.Our results proved that dietary supplement of GT and Se-GT remarkably improved the vascular functions and effectively prevented tissue damage by regulation of intestinal flora,and thus preventing hypertension induced by high-salt diet.

Blockade of Endogenous Angiotensin-(1–7) in Hypothalamic Paraventricular Nucleus Attenuates High Salt-Induced Sympathoexcitation and Hypertension

Angiotensin(Ang)-(1–7) is an important biologically-active peptide of the renin-angiotensin system. This study was designed to determine whether inhibition of Ang-(1–7) in the hypothalamic paraventricular nucleus(PVN) attenuates sympathetic activity and elevates blood pressure by modulating pro-inflammatory cytokines(PICs)and oxidative stress in the PVN in salt-induced hypertension. Rats were fed either a high-salt(8% NaCl) or a normal salt diet(0.3% NaCl) for 10 weeks, followed by bilateral microinjections of the Ang-(1–7) antagonist A-779 or vehicle into the PVN. We found that the mean arterial pressure(MAP), renal sympathetic nerve activity(RSNA), and plasma norepinephrine(NE) were significantly increased in salt-induced hypertensive rats. The high-salt diet also resulted in higher levels of the PICs interleukin-6, interleukin-1 beta, tumor necrosis factor alpha, and monocyte chemotactic protein-1, as well as higher gp91 phoxexpression and superoxide production in the PVN. Microinjection of A-779(3 nmol/50 nL) into the bilateral PVN of hypertensive rats not only attenuated MAP, RSNA, and NE, but also decreased the PICs and oxidative stress in the PVN. These results suggest that the increased MAP and sympathetic activity in salt-induced hypertension can be suppressed by blockade of endogenous Ang-(1–7) in the PVN, through modulation of PICs and oxidative stress.