Department of Nursing, The First Affiliated Hospital of Guangxi Medical University, No. 6, Shuangyong Road, Nanning, 530021, Guangxi, China.
BMC Cardiovasc Disord. 2021 Sep 16;21(1):440. doi: 10.1186/s12872-021-02233-w.
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.
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.
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.
Resistance exercise intervention downregulated miR-92a-3p expression, repaired oxidative stress injury and prevented CRT formation.
miR-92a-3p 和氧化应激与导管相关性血栓形成（CRT）有关。作为一种物理干预，抗阻运动可以有效促进血液循环。在这项研究中，我们研究了 miR-92a-3p、氧化应激和 P38 丝裂原活化蛋白激酶/核因子-κB（MAPK/NF-κB）通路在抗阻运动期间 CRT 中的作用。
采用大鼠 CRT 模型进行抗阻运动干预。此外，通过电子显微镜观察右颈静脉至右耳的病理变化。此外，通过 ELISA 检测大鼠血清中活性氧（ROS）的产生、丙二醛（MDA）的活性和血红素加氧酶（HO-1）的水平。通过实时定量 PCR 测定大鼠血管组织中 miR-92A-3p 和 HO-1 的表达水平。此外，通过 Western blot 分析大鼠静脉组织中 HO-1、NF-κB P65、p38MAPK 和 IκBa 的表达水平。
病理结果表明，CRT+RE 组的血栓发生率低于 CRT 组。在 CRT 组中，血清中与氧化应激相关的 ROS 和 MDA 标志物表达水平显著升高，而 HO-1 表达水平降低。在静脉组织中，miR-92a-3p 表达增加，HO-1 水平降低，p38MAPK 和 NF-κB p65 水平显著升高，而 P-IκBa 和 IκBa 水平显著降低。在 CRT+RE 组中，给予抗阻运动干预后，血清中 ROS 的产生和 MDA 的活性显著降低，HO-1 的表达水平增加，静脉组织中 miR-92a-3p 的表达水平显著降低，与 HO-1 呈负相关。p38MAPK 和 NF-κB p65 水平显著降低，而 P-IκBa 和 IκBa 水平显著升高。
抗阻运动干预下调 miR-92a-3p 表达，修复氧化应激损伤，防止 CRT 形成。
