丁蛋白通过介导心肌梗死后TGF-β1/Smad信号通路减轻心肌纤维化。

IF 2.2 4区生物学 Q3 CELL BIOLOGY

Journal of Molecular Histology Pub Date : 2025-10-22 DOI:10.1007/s10735-025-10641-x

Mengmeng Deng, Rui Ma, Jinlei Li, Pan Lu, Rong Tan, Zhen Chen, Xin Guo

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引用次数: 0

摘要

背景：心肌纤维化可加速心肌梗死（MI）后的心功能障碍。丁醛是一种查尔酮类化合物，具有多种生物学特性。然而，其对心肌梗死引起的心肌纤维化的影响尚不清楚。方法：采用左前降结扎法建立小鼠心肌梗死模型。TGF-β1刺激体外培养人心脏成纤维细胞（HCFs）。通过测定EF和FS来评价小鼠心功能。马森三色染色显示小鼠心脏纤维化区。Western blotting评估纤维化标志物和信号相关标志物的蛋白水平。CCK-8、EdU和Transwell检测HCF的增殖和迁移。结果：丁蛋白改善心肌梗死引起的心功能障碍，减少心肌纤维化面积。在MI小鼠和TGF-β1刺激的hcf中，Butein灭活TGF-β1/Smad信号。Butein抑制TGF-β1诱导的hcf增殖、迁移和胶原合成，其作用与TGF-β信号的药理抑制剂LY2109761相似。结论：丁蛋白通过灭活TGF-β1/Smad信号通路，抑制心肌纤维化和ECM沉积，从而减轻心肌梗死的发生。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Butein attenuates cardiac fibrosis by mediating TGF-β1/Smad signaling pathway after myocardial infarction

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Butein attenuates cardiac fibrosis by mediating TGF-β1/Smad signaling pathway after myocardial infarction

Background

Myocardial fibrosis has been found to accelerate heart dysfunction after myocardial infarction (MI). Butein is a chalcone compound possessing multiple biological properties. However, its effect on MI-induced myocardial fibrosis remains unclear.

Methods

A mouse MI model was established by left anterior descending ligation. Human cardiac fibroblasts (HCFs) were stimulated with TGF-β1 in vitro. Mouse cardiac function was evaluated by assessing EF and FS. Masson’s trichrome staining showed the fibrosis area in murine hearts. Western blotting evaluated protein levels of fibrosis markers and signaling-related markers. CCK-8, EdU, and Transwell assays were used to evaluate HCF proliferation and migration.

Results

Butein improved MI-induced cardiac dysfunction and reduced the fibrosis area in mice. Butein inactivated TGF-β1/Smad signaling in MI mice and TGF-β1-stimulated HCFs. Butein inhibited TGF-β1-induced proliferation, migration, and collagen synthesis in HCFs, which were similar to the effects of LY2109761, a pharmacological inhibitor of TGF-β signaling.

Conclusion

Butein mitigated MI development by inhibiting cardiac fibrosis and ECM deposition by inactivating the TGF-β1/Smad signaling pathway.

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来源期刊

Journal of Molecular Histology 生物-细胞生物学

CiteScore

5.90

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.