This preprint is under consideration at BMC Cardiovascular Disorders. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
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Research Article
Yanping Ying
First Affiliated Hospital of GuangXi Medical University
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
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.
Keywords
catheter-related thrombosis, resistance exercise intervention, miR-92A-3P, oxidative stress, MAPK/NF-κB pathway
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CURRENT STATUS: Under Review
Version 1
Posted 05 Jan, 2021
No community comments so far
Editorial decision: Major revision
On 09 Apr, 2021
Reviews received
Received 03 Apr, 2021
Reviewers agreed
On 10 Mar, 2021
Reviews received
Received 14 Feb, 2021
Reviewers agreed
On 19 Jan, 2021
Reviewers invited
Invitations sent on 12 Jan, 2021
Editor assigned
On 08 Jan, 2021
Editor invited
On 01 Jan, 2021
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On 01 Jan, 2021
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On 29 Dec, 2020
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This preprint is under consideration at BMC Cardiovascular Disorders. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Yanping Ying
First Affiliated Hospital of GuangXi Medical University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 05 Jan, 2021
No community comments so far
Editorial decision: Major revision
On 09 Apr, 2021
Reviews received
Received 03 Apr, 2021
Reviewers agreed
On 10 Mar, 2021
Reviews received
Received 14 Feb, 2021
Reviewers agreed
On 19 Jan, 2021
Reviewers invited
Invitations sent on 12 Jan, 2021
Editor assigned
On 08 Jan, 2021
Editor invited
On 01 Jan, 2021
Submission checks complete
On 01 Jan, 2021
First submitted
On 29 Dec, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
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.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
This preprint is available for download as a PDF.
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