Resistance exercise affects catheter-related thrombosis in rats through miR-92a-3p, oxidative stress and the MAPK/NF-κB pathway

Abstract

Background MiR-92a-3p and oxidative stress are associated with catheter-related thrombosis (CRT). As a kind of physical intervention, resistance exercise can effectively promote blood circulation. In this study, we investigated the roles of miR-92a-3p, oxidative stress and the P38 mitogen-activated protein kinase/nuclear factor-κB (MAPK/NF-κB) pathway in CRT during resistance exercise. Methods The rat CRT model was used for resistance exercise intervention. Moreover, pathological changes from the right jugular vein to the right auricle were observed under an electron microscope. In addition, reactive oxygen species (ROS) production, malondialdehyde (MDA) activity and heme oxygenase (HO-1) level in rat serum were detected via ELISA. The expression levels of miR-92A-3p and HO-1 in the vascular tissues of the rats were determined via real-time quantitative PCR. Additionally, the expression levels of HO-1, NF-κB P65, p38MAPK and IκBa in the venous tissues of the rats were analysed by Western blot analysis. Results The pathological results showed that the thrombosis incidence rate in the CRT + RE group was lower than that in the CRT group. In the CRT group, the expression levels of ROS and MDA, which are markers related to oxidative stress in serum, significantly increased whilst the expression of HO-1 decreased. In the venous tissue, the expression of miR-92a-3p increased, the level of HO-1 decreased, the levels of p38MAPK and NF-κB p65 significantly increased but that of P-IκBa and IκBa significantly decreased. In the CRT + RE group, after administering the resistance exercise intervention, ROS production and MDA activity in serum significantly decreased, the expression level of HO-1 increased and the expression level of miR-92a-3p in the venous tissues significantly decreased and was negatively correlated with that of HO-1. The levels of p38MAPK and NF-κB p65 significantly decreased but that of P- IκBa and IκBa significantly increased. Conclusion Resistance exercise intervention downregulated miR-92a-3p expression, repaired oxidative stress injury and prevented CRT formation.

Network pharmacology prediction and molecular docking-based strategy to discover the potential pharmacological mechanism of Huang–Qi–Gui–Zhi–Wu–Wu decoction against deep vein thrombosis

“…Studies have demonstrated that a sustained increase in reactive oxygen species can activate inflammatory reactions by activating MAPK signaling pathways. This activation leads to apoptosis of vascular endothelial cells and induces thrombosis [ 83 ]. Furthermore, studies have shown that ginsenoside-Rp3 can regulate MAPK signaling pathways to inhibit platelet activation and thrombosis [ 84 ].…”

Endurance-dependent urinary extracellular vesicle signature: shape, metabolic miRNAs, and purine content distinguish triathletes from inactive people

“…In the present study, we also observed downregulation of EV miR-92a-3p and miR-27a-3p in TR compared to IN individuals. As reported by Wen and colleagues ([ 50 ], p. 3), the reduction in circulating miR-92a-3p may be induced by resistance exercise intervention that leads to a decreased oxidative stress response. This mechanism seems to be related to a reduction of miR-92a-3p-mediated repression of HO-1 (HMOX1), an antioxidant enzyme found in vascular endothelial cells and smooth muscle cells.…”

Advances in oxidative stress in pathogenesis of diabetic kidney disease and efficacy of TCM intervention

“…In normal cases, NF-кB is ubiquitously present in various tissue cells in an inactive state. In response to stimulation with activators (e.g., proinflammatory cytokine, Toll-like receptor, p38-MAPK, HO-1, and ROS), NF-κB dimers will be released to nucleus to regulate target gene expression, inducing the body’s immune and inflammatory responses [ 34 ]. Multiple studies have proved that DKD development is associated with NF-κB hyper-activation.…”