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阿托伐他汀对Notch1-TGF-β-Smads信号通路的失活作用改善急性心肌梗死大鼠的心功能和血流动力学性能

Inactivation of Notch1-TGF-β-Smads Signaling Pathway by Atorvastatin Improves Cardiac Function and Hemodynamic Performance in Acute Myocardial Infarction Rats.

作者信息

Kang Qi, Kang Mei, Yang Mengyun, Fernando Taniya

机构信息

Department of Cardiology, Tianjin Medical University General Hospital, Tianjin, China.

Postgraduate College, The first Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

出版信息

J Vasc Res. 2025;62(3):133-144. doi: 10.1159/000542728. Epub 2025 Jan 27.

DOI:10.1159/000542728
PMID:39870054
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12136607/
Abstract

INTRODUCTION

The aim of this study was to determine the effects of atorvastatin on cardiac function and hemodynamics and to investigate its functional mechanism on cardiac fibrosis in acute myocardial infarction (AMI) rats.

METHODS

Cardiac functions and hemodynamic changes were evaluated in each group on day 28. Quantitative reverse transcription-polymerase chain reaction, Western blot, and immunohistochemistry were performed to detect the expression of notch1, transforming growth factor-β (TGF-β), Smad2, Smad7, as well as myocardial fibrosis factors (i.e., collagen I, collagen III, and galectin-3) in the myocardial tissues of AMI rats. The changes of myocardial cell structure and myocardial collagen fibers of AMI rats were observed with hematoxylin and eosin staining and Masson staining.

RESULTS

Atorvastatin improved the cardiac function and hemodynamic performance. Atorvastatin downregulated the expression of notch1, smad2, collagen I, and collagen III in AMI rats. Atorvastatin treatment decreased the transcription of notch1, TGF-β, and smad2, while it increased smad7 in AMI rats. Atorvastatin induced the downregulation of collagen I, collagen III, and galectin-3. Myocardial immunohistochemical analysis showed atorvastatin inhibited the expression of notch1, TGF-β, and smad2 in myocardial tissues.

CONCLUSION

Atorvastatin inhibited myocardial fibrosis by interfering with notch1-TGF-β-smads signal pathways. In addition, it could mitigate myocardial remodeling and improve cardiac functions and hemodynamics.

摘要

引言

本研究旨在确定阿托伐他汀对急性心肌梗死（AMI）大鼠心功能和血流动力学的影响，并探讨其对心肌纤维化的作用机制。

方法

在第28天评估每组的心脏功能和血流动力学变化。采用定量逆转录-聚合酶链反应、蛋白质印迹法和免疫组织化学法检测AMI大鼠心肌组织中Notch1、转化生长因子-β（TGF-β）、Smad2、Smad7以及心肌纤维化因子（即I型胶原、III型胶原和半乳糖凝集素-3）的表达。用苏木精-伊红染色和Masson染色观察AMI大鼠心肌细胞结构和心肌胶原纤维的变化。

结果

阿托伐他汀改善了心脏功能和血流动力学性能。阿托伐他汀下调了AMI大鼠中Notch1、Smad2、I型胶原和III型胶原的表达。阿托伐他汀治疗降低了AMI大鼠中Notch1、TGF-β和Smad2的转录，同时增加了Smad7的转录。阿托伐他汀诱导I型胶原、III型胶原和半乳糖凝集素-3的下调。心肌免疫组织化学分析显示阿托伐他汀抑制了心肌组织中Notch1、TGF-β和Smad2的表达。

结论

阿托伐他汀通过干扰Notch1-TGF-β-Smads信号通路抑制心肌纤维化。此外，它还可以减轻心肌重构，改善心脏功能和血流动力学。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/711663abc06e/jvr-2025-0062-0003-542728_F07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/533b3f7b5012/jvr-2025-0062-0003-542728_F01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/e342351e58f7/jvr-2025-0062-0003-542728_F02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/ae2404d70f0c/jvr-2025-0062-0003-542728_F03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/8a26e2700fad/jvr-2025-0062-0003-542728_F04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/f3f5d3091a96/jvr-2025-0062-0003-542728_F05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/c7ff5ad61557/jvr-2025-0062-0003-542728_F06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/711663abc06e/jvr-2025-0062-0003-542728_F07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/533b3f7b5012/jvr-2025-0062-0003-542728_F01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/e342351e58f7/jvr-2025-0062-0003-542728_F02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/ae2404d70f0c/jvr-2025-0062-0003-542728_F03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/8a26e2700fad/jvr-2025-0062-0003-542728_F04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/f3f5d3091a96/jvr-2025-0062-0003-542728_F05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/c7ff5ad61557/jvr-2025-0062-0003-542728_F06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb20/12136607/711663abc06e/jvr-2025-0062-0003-542728_F07.jpg

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