Stanisic Jelena, Koricanac Goran, Culafic Tijana, Romic Snjezana, Stojiljkovic Mojca, Kostic Milan, Ivkovic Tamara, Tepavcevic Snezana
Laboratory for Molecular Biology and Endocrinology, Vinča Institute of Nuclear Sciences, National Institute of the Republic of Serbia, University of Belgrade, P.O. Box 522, 11001, Belgrade, Serbia.
Mol Cell Biochem. 2025 Apr 17. doi: 10.1007/s11010-025-05288-x.
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.
我们之前发表的研究结果已证明，低强度运动（相当于快走）对控制断奶后雄性大鼠在高糖饮食下的心脏胰岛素抵抗有益。不过，其在预防心脏炎症方面的作用尚不清楚。本实验旨在研究低强度运动对断奶后暴露于高糖饮食（10%）的雄性大鼠心脏炎症的预防作用。雄性Wistar大鼠被随机分为久坐对照组、高糖超载久坐组和高糖超载且进行九周跑步机运动的组。测定了心脏诱导型一氧化氮合酶（iNOS）、基质金属蛋白酶9的蛋白表达，以及核因子κB（NF-κB）的细胞定位/磷酸化，还有钠钾ATP酶泵（Na/K-ATPase）的α1和α2亚基。此外，检测了肿瘤坏死因子α（TNFα）和细胞因子信号转导抑制因子3（SOCS3）的基因表达。结果表明，久坐大鼠的慢性高糖饮食会提高关键炎症标志物的表达，包括SOCS3、TNFα、NF-κB和iNOS，以及质膜α1和α2亚基。运动可预防高糖饮食引起的改变，但iNOS表达除外。此外，运动增加了高糖喂养大鼠裂解物中Na/K-ATPaseα1和α2亚基的蛋白表达。这些发现表明，低强度运动是一种有效的非侵入性心脏保护策略，有助于通过调节断奶后雄性大鼠胰岛素抵抗心脏中的TNFα和NF-κB表达来预防炎症。
