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.
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Posted 11 Mar, 2021
On 06 Mar, 2021
Invitations sent on 06 Mar, 2021
Received 06 Mar, 2021
Received 06 Mar, 2021
On 04 Mar, 2021
On 04 Mar, 2021
On 04 Mar, 2021
On 23 Feb, 2021
Posted 11 Mar, 2021
On 06 Mar, 2021
Invitations sent on 06 Mar, 2021
Received 06 Mar, 2021
Received 06 Mar, 2021
On 04 Mar, 2021
On 04 Mar, 2021
On 04 Mar, 2021
On 23 Feb, 2021
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
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