Abstract
BackgroundMiR-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.MethodsThe 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.ResultsThe 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.ConclusionResistance exercise intervention downregulated miR-92a-3p expression, repaired oxidative stress injury and prevented CRT formation.
Highlights
Central venous catheters (CVCs) are extensively applied in medical and health institutions
This study investigated the mechanism by which oxidative stress and miR-92a-3p prevent catheter-related thrombosis (CRT) in rats
The present study proved that anti-resistance exercises changed blood flow shear stress, inhibited endothelial cells to repair oxidative stress and reduced reactive oxygen species (ROS) production, thereby improving the function of vascular endothelium and, to a certain extent, playing a role in preventing venous thrombosis [41, 42]
Summary
Central venous catheters (CVCs) are extensively applied in medical and health institutions. Recent studies noted that 16–18% of patients with CVCs have evidence of CRT as revealed by ultrasound or intravenous screening [4]. CRT cannot be detected without ultrasonic evaluation and testing, and compounding this problem is the fact that only 1–5% of patients are symptomatic [6]. CRT can be characterised as a ‘high risk, common’ disease. CRT can increase pain sensitivity, leading to catheter dysfunction, increased risks of infection and central venous stenosis; it increases the length of hospital stay and medical costs [7]. MiR-92a-3p and oxidative stress are associated with catheter-related thrombosis (CRT). 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
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
