Low-intensity exercise prevents cardiac inflammation through the NF-κB/TNFα pathway in insulin-resistant male rats.

Abstract

Our previously published results have proven that low-intensity exercise, equivalent to brisk walking, is beneficial in managing cardiac insulin resistance in post-weaning male rats exposed to a fructose-rich diet. Still, its role in protecting against cardiac inflammation is unclear. This experiment was designed to investigate the preventive effect of low-intensity exercise on cardiac inflammation in male post-weaning rats exposed to a fructose-rich diet (10%). Male Wistar rats were randomly assigned to a sedentary control group, a sedentary group with fructose overload, and a fructose overload group subjected to treadmill exercise for nine weeks. Protein expression of cardiac inducible nitric oxide synthase (iNOS), matrix metalloproteinase 9, as well as cellular localization/phosphorylation of nuclear factor kappa B (NF-κB), and α1 and α2 subunits of sodium-potassium ATPase pump (Na/K-ATPase) was determined. Additionally, gene expression of tumor necrosis factor α (TNFα) and suppressor of cytokine signaling 3 (SOCS3) was examined. The results demonstrate that a chronic fructose-rich diet in sedentary rats elevates the expression of key inflammatory markers, including SOCS3, TNFα, NF-κB, and iNOS, as well as the plasma membrane α1 and α2 subunits. Exercise prevented alterations induced by a fructose-rich diet, except iNOS expression. Additionally, exercise increased the protein expression of the α1 and α2 subunits of Na/K-ATPase in the lysate of fructose-fed rats. These findings suggest that low-intensity exercise is an effective non-invasive strategy for cardioprotection, helping to prevent inflammation by modulating TNFα and NF-κB expression in insulin-resistant hearts of post-weaning male rats.