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- Title
Salvianolic acid B ameliorates myocardial fibrosis in diabetic cardiomyopathy by deubiquitinating Smad7.
- Authors
Luo, Hong; Fu, Lingyun; Wang, Xueting; Yini Xu; Ling Tao; Shen, Xiangchun
- Abstract
Background: Salvianolic acid B (Sal B), a water-soluble phenolic compound derived from Salvia miltiorrhiza Bunge, is commonly used in Traditional Chinese Medicine to treat cardiovascular disease. In our previous study, Sal B protected against myocardial fibrosis induced by diabetic cardiomyopathy (DCM). This study aimed to investigate the ameliorative effects and potential mechanisms of Sal B in mitigating myocardial fibrosis induced by DCM. Methods: Various methods were used to investigate the effects of Sal B on myocardial fibrosis induced by DCM in vivo and in vitro. These methods included blood glucose measurement, echocardiography, HE staining, Masson's trichrome staining, Sirius red staining, cell proliferation assessment, determination of hydroxyproline levels, immunohistochemical staining, evaluation of fibrosis-related protein expression (Collagen-I, Collagen-III, TGF-β1, p-Smad3, Smad3, Smad7, and α-smooth muscle actin), analysis of Smad7 gene expression, and analysis of Smad7 ubiquitin modification. Results: The animal test results indicated that Sal B significantly improved cardiac function, inhibited collagen deposition and phenotypic transformation, and ameliorated myocardial fibrosis in DCM by upregulating Smad7, thereby inhibiting the TGF-β1 signaling pathway. In addition, cell experiments demonstrated that Sal B significantly inhibited the proliferation, migration, phenotypic transformation, and collagen secretion of cardiac fibroblasts (CFs) induced by high glucose (HG). Sal B significantly decreased the ubiquitination of Smad7 and stabilized the protein expression of Smad7, thereby increasing the protein expression of Smad7 in CFs and inhibiting the TGF-β1 signaling pathway, which may be the potential mechanism by which Sal B mitigates myocardial fibrosis induced by DCM. Conclusion: This study revealed that Sal B can improve myocardial fibrosis in DCM by deubiquitinating Smad7, stabilizing the protein expression of Smad7, and blocking the TGF-β1 signaling pathway.
- Subjects
IN vitro studies; ECHOCARDIOGRAPHY; COLLAGEN; TRANSFORMING growth factors-beta; STATISTICS; DIABETIC cardiomyopathy; HERBAL medicine; IN vivo studies; STAINS &; staining (Microscopy); FIBROBLASTS; ANALYSIS of variance; CARDIOMYOPATHIES; ANIMAL experimentation; IMMUNOHISTOCHEMISTRY; HEART; WESTERN immunoblotting; FIBROSIS; BLOOD sugar; PRECIPITIN tests; GENE expression; CELLULAR signal transduction; CELL motility; RATS; CELL proliferation; FLUORESCENT antibody technique; DESCRIPTIVE statistics; RESEARCH funding; POLYMERASE chain reaction; DATA analysis software; DATA analysis; CHINESE medicine; CARRIER proteins; MICE; DISEASE complications
- Publication
Chinese Medicine, 2023, Vol 18, Issue 1, p1
- ISSN
1749-8546
- Publication type
Article
- DOI
10.1186/s13020-023-00868-9