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.

中文翻译：

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抗阻运动通过 miR-92a-3p、氧化应激和 MAPK/NF-κB 通路影响大鼠导管相关血栓形成

MiR-92a-3p 和氧化应激与导管相关血栓形成 (CRT) 相关。抗阻运动作为一种物理干预，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 CRT 中在抗阻运动中的作用。大鼠CRT模型用于阻力运动干预。电镜下观察右颈静脉至右耳廓的病理变化。此外，通过ELISA检测大鼠血清中活性氧（ROS）产生、丙二醛（MDA）活性和血红素加氧酶（HO-1）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。病理结果显示，CRT+RE组血栓发生率低于CRT组。在 CRT 组中，血清中与氧化应激相关的标志物 ROS 和 MDA 的表达水平显着增加，而 HO-1 的表达水平降低。静脉组织中miR-92a-3p表达升高，HO-1水平降低，p38MAPK和NF-κB p65水平显着升高，P-IκBa和IκBa显着降低。在 CRT + RE 组中，抗阻运动干预后，血清中 ROS 的产生和 MDA 活性显着降低，静脉组织中HO-1的表达水平升高，miR-92a-3p的表达水平显着降低，与HO-1的表达水平呈负相关。p38MAPK 和 NF-κB p65 水平显着降低，但 P-IκBa 和 IκBa 水平显着升高。抗阻运动干预下调 miR-92a-3p 表达，修复氧化应激损伤并阻止 CRT 形成。