This preprint is under consideration at Journal of Cardiothoracic Surgery. 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
Xiao Liang
Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Nangang District, Harbin, 150000, China
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Objective: Cardiovascular diseases impose a considerable economic burden on health services and remain a threat to human being. (-)-Epicatechin [(-)-EPI], a traditional Chinese medicine is applied to treatment against the cardiovascular diseases. Herein, we aimed at investigating the underlying mechanism whereby (-)-EPI affects myocardial fibrosis (MF).
Methods: The efficacy of (-)-EPI was determined in mouse models of acute myocardial infarction (AMI) and hypoxia-treated fibroblasts. Western blot and RT-qPCR analyses were conducted to determine TGF-β1, SMAD2 and SMAD3 expression, as collagen content was detected. CCK-8 assay and flow cytometry were carried out to detect fibroblast proliferation and apoptosis. HE and Masson staining reflected the histological change of myocardial tissues
Results: Compared to sham-operated mice, AMI group exhibited MF and hypoxia-treated cardiac fibroblasts proliferation was restrained and apoptosis was increased. Treatment with (-)-EPI significantly attenuated the MF condition and restored fibroblast proliferation and apoptosis, whereas these effects were abrogated by the TGF-β1 agonist HY-100347A. (-)-EPI administration caused a decline in TGF-β1, SMAD2 and SMAD3 expression. Mechanistically, (-)-EPI targeting TGF-β signaling inhibits collagen deposition and attenuates MF.
Conclusion: Collectively, (-)-EPI could improve MF following AMI through down-regulation of TGF-β1 signaling, providing a novel insight into treatment against the cardiovascular diseases.
Keywords
Acute myocardial infarction, Myocardial fibrosis, (-)-Epicatechin, TGF-β1, Cardiovascular
Figure 1
Figure 2
Figure 3
Figure 4
Loading...
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 11 Mar, 2021
No community comments so far
Reviewer #1 agreed
On 06 Mar, 2021
Reviewers invited
Invitations sent on 06 Mar, 2021
Review #? received
Received 06 Mar, 2021
Review #1 received
Received 06 Mar, 2021
Editor assigned
On 04 Mar, 2021
Submission checks complete
On 04 Mar, 2021
Editor invited
On 04 Mar, 2021
First submitted
On 23 Feb, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cardiothoracic Surgery
Learn more about our company.
This preprint is under consideration at Journal of Cardiothoracic Surgery. 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
Xiao Liang
Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng Street, Nangang District, Harbin, 150000, China
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 11 Mar, 2021
No community comments so far
Reviewer #1 agreed
On 06 Mar, 2021
Reviewers invited
Invitations sent on 06 Mar, 2021
Review #? received
Received 06 Mar, 2021
Review #1 received
Received 06 Mar, 2021
Editor assigned
On 04 Mar, 2021
Submission checks complete
On 04 Mar, 2021
Editor invited
On 04 Mar, 2021
First submitted
On 23 Feb, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cardiothoracic Surgery
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Objective: Cardiovascular diseases impose a considerable economic burden on health services and remain a threat to human being. (-)-Epicatechin [(-)-EPI], a traditional Chinese medicine is applied to treatment against the cardiovascular diseases. Herein, we aimed at investigating the underlying mechanism whereby (-)-EPI affects myocardial fibrosis (MF).
Methods: The efficacy of (-)-EPI was determined in mouse models of acute myocardial infarction (AMI) and hypoxia-treated fibroblasts. Western blot and RT-qPCR analyses were conducted to determine TGF-β1, SMAD2 and SMAD3 expression, as collagen content was detected. CCK-8 assay and flow cytometry were carried out to detect fibroblast proliferation and apoptosis. HE and Masson staining reflected the histological change of myocardial tissues
Results: Compared to sham-operated mice, AMI group exhibited MF and hypoxia-treated cardiac fibroblasts proliferation was restrained and apoptosis was increased. Treatment with (-)-EPI significantly attenuated the MF condition and restored fibroblast proliferation and apoptosis, whereas these effects were abrogated by the TGF-β1 agonist HY-100347A. (-)-EPI administration caused a decline in TGF-β1, SMAD2 and SMAD3 expression. Mechanistically, (-)-EPI targeting TGF-β signaling inhibits collagen deposition and attenuates MF.
Conclusion: Collectively, (-)-EPI could improve MF following AMI through down-regulation of TGF-β1 signaling, providing a novel insight into treatment against the cardiovascular diseases.
Figure 1
Figure 2
Figure 3
Figure 4
Loading...