2. Academic Validation
  3. Butein attenuates cardiac fibrosis by mediating TGF-β1/Smad signaling pathway after myocardial infarction

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

  • J Mol Histol. 2025 Oct 22;56(6):352. doi: 10.1007/s10735-025-10641-x.
Mengmeng Deng # 1,  Rui Ma # 2,  Jinlei Li # 3,  Pan Lu 1,  Rong Tan 1,  Zhen Chen 4,  Xin Guo 5
Affiliations

Affiliations

  • 1 Department of Cardiology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430000, Hubei Province, People's Republic of China.
  • 2 Sinopharm Dongfeng General Hospital, Shiyan, 442000, China.
  • 3 School of Medicine, Jianghan University, Wuhan, 430000, China.
  • 4 Department of Emergency, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, No.26 Shengli Street, Jiang' an District, Wuhan, 430000, Hubei Province, People's Republic of China. [email protected].
  • 5 Department of Cardiology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430000, Hubei Province, People's Republic of China. [email protected].
  • # Contributed equally.
PMID: 41123714 DOI: 10.1007/s10735-025-10641-x
Abstract

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.

Keywords

Butein; Collagen; Fibrosis; MI; TGF-β1.

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