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 on 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. Furthermore, expression levels of miR-92A-3p and HO-1 in the vascular tissues of the rats were detected via real-time quantitative PCR. Additionally, expression levels of HO-1, NF-κB P65, p38MAPK, and IκBa in the venous tissues of the rats were analyzed by Western blot analysis.
Results: Thrombosis incidence rate in CRT+RE group was lower than that in CRT group. In the thrombosis model, markers related to oxidative stress and miR-92a-3p increased. After administering the resistance exercise intervention, ROS production and MDA activity significantly decreased, the expression level of HO-1 increased, and the expression level of miR-92A-3p in the vascular tissues significantly decreased. The levels of p38MAPK and NF-κB p65 significantly decreased but that of IκBa significantly increased.
Conclusion: Resistance exercise intervention downregulated miR-92a-3p expression, repaired oxidative stress injury, and prevented CRT formation.