Exercise training augments Sirt1-signaling and attenuates cardiac inflammation in D-galactose induced-aging rats

Abstract

Exercise is known to be beneficial in controlling aging associated disorders however, the consequence of long-term exercise on cardiac health among aging population is not much clear. In this study the protective effect of exercise on aging associated cardiac disorders was determined using a D-galactose-induced aging model. Eight weeks old Sprague Dawley rats were given intraperitoneal injection of 150 mL/kg D-galactose. Swimming exercise was provided in warm water for 60 min/day for five days per week. Hematoxylin and eosin staining of cardiac tissue sections revealed cardiomyocyte disarrangements in the aging rat hearts but long-term exercise training showed improvements in the cardiac histology. Exercise training also enhanced the expression levels of proteins such as SIRT1, PGC-1α and AMPKα1 that are associated with energy homeostasis and further suppressed aging associated inflammatory cytokines. Our results show that long-term exercise training potentially enhances SIRT1 associated anti-aging signaling and provide cardio-protection against aging.

The effect of swimming exercise and diet on the hypothalamic inflammation of ApoE-/- mice based on SIRT1-NF-κB-GnRH expression

“…Swimming exercise relieves the peripheral and central inflammation, but the mechanism has not been investigated extensively to date. It is reported that SIRT1 can inhibit nuclear factor kappa B (NF-κB) signaling pathway and suppress the systemic inflammation [11,12,31]. The NF-κB is composed of two subunits, P50 and P65, and is activated by various inflammatory cytokines.…”

“…SIRT1 has various physiological functions by regulating some key targets via deacetylation, such as NF-κB and peroxisome proliferator-activated receptor γ (PPARγ) [11]. Chen WK et al [12] demonstrated that long-term aerobic exercise facilitated SIRT1 protein expression and enhanced SIRT1-related anti-aging signals. Aerobic exercise induced the expression of SIRT1 which inhibited the NF-κB pathway.…”

Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging

“…Under oxidative stress conditions, the Foxo3a existing in the nucleus induces the expression of inflammatory proteins. SIRT1 protects the cell and stabilizes nDNA by deacetylating Foxo3a and attenuating its function [104] (Figure 4). SRT1720, an activator of SIRT1, ameliorates contractile dysfunction and impaired mitophagy in cardiac aging [105].…”

Extracellular vesicles in cardiovascular diseases

“…Long-term exercise-derived circulating EVs protect the heart from myocardial ischaemia/reperfusion injury via exosomal miR-342-5p 44 . Long-term exercise training potentially enhances silent information regulator 1 (SIRT1) signalling, attenuates cardiac inflammation, and provides cardioprotection in d -galactose-induced ageing rats 45 . Cigarette smoke-induced EVs promote thrombin generation in normal human plasma and contribute to increased cardiovascular risk in smokers 46 .…”