Taohong siwu decoction attenuates myocardial fibrosis by inhibiting fibrosis proliferation and collagen deposition via TGFBR1 signaling pathway

2021 ◽  
Vol 270 ◽  
pp. 113838
Author(s):  
Zhangbin Tan ◽  
Xiaoli Jiang ◽  
Wenyi Zhou ◽  
Bo Deng ◽  
Min Cai ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Myocardial Fibrosis ◽  
Collagen Deposition ◽  
Taohong Siwu Decoction

scholarly journals Modified citrus pectin ameliorates myocardial fibrosis and inflammation via suppressing galectin-3 and TLR4/MyD88/NF-κB signaling pathway

2020 ◽  
Vol 126 ◽  
pp. 110071 ◽  
Author(s):  
Geng-Rui Xu ◽  
Chuang Zhang ◽  
Hong-Xia Yang ◽  
Jia-Huan Sun ◽  
Yue Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Myocardial Fibrosis ◽  
Citrus Pectin ◽  
Galectin 3

Abstract P168: Activated Protein C Inhibits the Development of Myocardial Fibrosis

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Mryanda J Sopel ◽  
Tanya L Myers ◽  
Timothy D Lee ◽  
Robert S Liwski ◽  
Jean-Francois Legare
Keyword(s):  
Cardiovascular Diseases ◽  
Myocardial Fibrosis ◽  
Adhesion Molecule ◽  
Protein C ◽  
Activated Protein C ◽  
Saline Control ◽  
Collagen Deposition ◽  
Cellular Infiltration ◽  
Fibrotic Response ◽  
Cellular Adhesion Molecule

Background: Activated Protein C (aPC) is a naturally produced circulating anticoagulant with anti-inflammatory and cytoprotective properties proposed to have beneficial effects on the myocardium. Myocardial fibrosis is a pathophysiologic process evident in many cardiovascular diseases and is believed to directly contribute to eventual organ failure. Using a well-described model of myocardial fibrosis after Angiotensin II (AngII) infusion our aim was to investigate the novel therapeutic function of aPC in the development of fibrosis. Methods: C57Bl/6 mice were continuously infused with AngII (2.0 μ g/kg/min), AngII and aPC (0.4 μ g/kg/min), or saline for a 3d period. Hearts were harvested and processed for analysis. Cellular infiltration and collagen deposition were analyzed using histologic staining. Cellular apoptosis was assessed using a TUNEL assay. Quantitative RT-PCR was used to assess transcript levels of molecular mediators. Results: Infusion of AngII for 3d resulted in multifocal areas of myocardial cellular infiltration associated with significant collagen deposition compared to saline control animals (p≤0.01). The addition of aPC with AngII infusion inhibited this fibrotic response. Co-administration with aPC also inhibited the upregulation of the pro-fibrotic cytokine CTGF expression seen in AngII infused animals (p≤0.01). Apoptosis was also significantly inhibited when aPC was co-administered based on a decrease of in TUNEL positive cells and an increase expression ration of BCL/BAX suggesting an anti-apoptotic effect (p≤0.01), Furthermore, aPC also inhibited the up-regulation of the cell adhesion molecule p-selectin seen in AngII infused animals (p≤0.01). Conclusion: The co-administration of aPC in a model of myocardial fibrosis was able to abrogate completely the fibrotic response. The mechanism of action of aPC appears to be a decreased cellular adhesion molecule expression in the myocardium leading to decreased cellular infiltration and enhanced cellular survival. This data suggests that aPC has the potential as a therapeutic agent in cardiovascular diseases.

Maternal endotoxemia induces renal collagen deposition in adult offspring: Role of NADPH oxidase/TGF-β1/MMP-2 signaling pathway

2020 ◽  
Vol 684 ◽  
pp. 108306 ◽  
Author(s):  
Juliane S. Farias ◽  
Kelly M. Santos ◽  
Natália K.S. Lima ◽  
Edjair V. Cabral ◽  
Regina S. Aires ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Signaling Pathway ◽  
Adult Offspring ◽  
Collagen Deposition ◽  
Tgf Β1

QiShenYiQi Pills® ameliorates ischemia/reperfusion-induced myocardial fibrosis involving RP S19-mediated TGFβ1/Smads signaling pathway

2019 ◽  
Vol 146 ◽  
pp. 104272 ◽  
Author(s):  
Qian-Ning Zheng ◽  
Xiao-Hong Wei ◽  
Chun-Shui Pan ◽  
Quan Li ◽  
Yu-Ying Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Myocardial Fibrosis ◽  
Ischemia Reperfusion

AB23A Reduces TGF-β1-Induced Human Cardiac Fibroblasts (HCF) Proliferation and Collagen Secretion via MER/ERK1/2/CREB Pathway

2020 ◽  
Vol 10 (6) ◽  
pp. 798-803
Author(s):  
Dinghui Hu ◽  
Yanhu Wu ◽  
Jin Du ◽  
Hang Li ◽  
Zuntao Liu
Keyword(s):  
Western Blot ◽  
Signaling Pathway ◽  
Myocardial Fibrosis ◽  
Cardiac Fibroblasts ◽  
Heart Diseases ◽  
Protein Levels ◽  
Collagen Secretion ◽  
Assay Result ◽  
Human Cardiac Fibroblasts ◽  
Creb Pathway

Background and Objectives: Myocardial fibrosis is associated with many forms of heart diseases which is characterized by the accumulation of activated cardiac fibroblasts (CFBs) and excess deposition of extracellular matrix (ECM). Natural compounds such as Alisol B 23-acetate has been proved to maintain the activation of ERK1/2, but whether it can affect cardiac fibroblasts by MER/ERK1/2/CREB signaling pathway is still unknown. Methods: The cell was identified with α-SMA protein level detected by immunofluorescence staining method. The cell proliferation was examined by CCK8 assay. Col I and Col III protein levels were examined by western blot and sirius red staining to detect the ECM level. Furthermore, p-MERK, MERK, P-ERK, ERK and CREB were examined by western blot to verify whether Alisol could activate the MERK/ERK1/2/CREB pathway in myocardial fibrosis. Results: CCK8 assay result indicated that Alisol reduced the cell viability of CFBs induced by TGF-β1. In addition, Alisol significantly decreased the ECM deposition of CFBs. Furthermore, Alisol could activate MERK/ERK1/2/CREB signaling pathway. Conclusion: These results verified that Alisol inhibited myocardial fibrosis via MERK/ERK1/2/CREB pathway.

Urocortin attenuates myocardial fibrosis in diabetic rats via the Akt/GSK-3β signaling pathway

2016 ◽  
Vol 41 (2) ◽  
pp. 148-157 ◽  
Author(s):  
Xinyu Liu ◽  
Chunna Liu ◽  
Jian Li ◽  
Xiaoyan Zhang ◽  
Feiran Song ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Myocardial Fibrosis ◽  
Diabetic Rats ◽  
Gsk 3Β
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